Where Science and Faith Converge
  • Simple Biological Rules Affirm Creation

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | Sep 04, 2019

    “Biology is the study of complicated things that give the appearance of having been designed for a purpose.”
    –Richard Dawkins

    To say that biological systems are complicated is an understatement.

    When I was in college, I had some friends who avoided taking courses in the life sciences because of the complexity of biological systems. On the other hand, I found the complexity alluring. It’s what drew me to biochemistry. I love to immerse myself in the seemingly never-ending intricacies of biomolecular systems and try to make sense of them.

    Perhaps nothing exemplifies the daunting complexity of biochemistry more than intermediary metabolism.

    Order in the Midst of Biochemical Complexity

    I remember a conversation I had years ago with a first-year graduate student who worked in the same lab as me when I was a postdoc at the University of Virginia. He was complaining about all the memorization he had to do for the course he was taking on intermediary metabolism. How else was he going to become conversant with all the different metabolic routes in the cell?

    I told him that he was approaching his classwork in the wrong way. Despite the complexity and chemical diversity of the metabolic pathways in the cell, a set of principles exists that dictates the architecture and operation of metabolic routes. I encouraged my lab mate to learn these principles because, once he did, he would be able to use them to write out all of the metabolic routes with minimal memorization.

    These principles make sense of the complexity of intermediary metabolism. Are there similar rules that make sense of biological diversity and complexity?

    Rules Govern Biological Systems

    As it turns out, the insight I offered my lab mate may well have been prescient.

    The idea that a simple set of principles—rules, if you will—accounts for the complexity and diversity of biological systems may be more widespread than life scientists fully appreciate. At least it appears this way based on work carried out recently by researchers from Duke University.1 These investigators discovered a simple rule that predicts the behavior of mutually beneficial symbiotic relationships (mutualism) in ecosystems. Mutualistic interactions play an important and dominant role in ecosystem stability.

    The Duke University scientists’ accomplishment represents a significant milestone. Lingchong You, one of the study’s authors, points out the difficulty of finding rules that govern all biological systems:

    “In a perfect world, you’d be able to follow a simple set of molecular rules to understand how every biological system operated. But, in reality, it’s difficult to establish rules that encompass the immense diversity and complexity of biological systems. Even when we do establish general rules, it’s still challenging to use them to explain and quantify various physical properties.”2

    Yet, You and his collaborators have done just that for mutualism. Their insight moves biology closer to physics and chemistry where simple rules can account for the physical world. Their work holds the potential to open up new vistas in the life sciences that can lead to a deeper, more fundamental understanding of biological systems.

    In fact, the researchers think that simple rules dictating the operation of biological systems may not be an unusual feature of mutualistic interactions but may apply more broadly. They write, “Beyond establishing another simple rule . . . we also demonstrated that one can purposefully seek an appropriate abstraction level where a simple unifying rule emerges over system diversity.”3

    If the Duke University scientists’ insight generally applies to biological systems, it has interesting theological implications. If biological systems do, indeed, conform to a simple set of rules, it becomes more reasonable to think that a Creator played a role in the origin, history, and design of life.

    I’ll explain how in a moment, but first let’s take a look at some details of the Duke University investigators’ work.

    Mutualism and Ecosystem Stability

    Biological organisms often form symbiotic relationships. When these relationships benefit all of the organisms involved, it is called mutualism. These mutualistic relationships are vital to ecosystems and they directly and indirectly benefit humanity. For example, coral reefs depend on mutualistic interactions between coral and algae. In turn, reefs provide habitats for a diverse ensemble of organisms that support human life and flourishing.

    Unfortunately, mutualistic systems can collapse when one or more of the partners experiences stress or disappears from the ecosystem. A disruption in a relationship can lead to the loss of other members of the ecosystem, thereby altering the ecosystem’s composition and opening up niches for invading organisms. Sadly, this type of collapse is happening in coral reefs around the world today.

    Mutualism Can Be Explained by a Simple Rule

    To gain insight into the rules that dictate ecosystem stability and predict collapse (due to a loss of mutualistic relationships), the Duke University researchers sought to develop a framework that would allow them to determine the outcome of mutualistic interactions. For the predictive framework, the scientists wrote 52 mathematical equations, each one specifically describing one of the various forms of mutualism. These equations were based on a simple biological logic; namely, mutualism consists of two or more populations of organisms that produce a benefit (B) for all the organisms that reduces the stress (S) they experience at a cost (C).

    Mathematical analysis of these equations allowed the researchers to discover a simple inequality that governs the transition from coexistence to collapse. As it turns out, mutualistic interactions remain stable when B > S, and they collapse when this inequality is not observed. Though intuitive, it is still remarkable that this simple relationship dictates the behavior of all types of mutualism.

    The researchers learned that determining the value of S is relatively straightforward. On the other hand, quantifying B proves to be a challenge due to the large number of variables such as temperature, nutrient availability, genetic variation, etc., that influence mutualistic interactions. To work around this problem, the researchers developed a machine-learning algorithm that could calculate B using the input of a large number of variables.

    This work has obvious importance for ecologists as ecosystems all over the planet face collapse. Beyond that, it has important theological implications when we recognize that a simple mathematical equation governs the behavior of mutualistic relationships among organisms.

    Let me explain.

    The Case for a Creator

    From my vantage point, one of the most intriguing aspects of our universe is its intelligibility and our capacity as human beings to make sense of the world around us—quite often, through the use of simple rules we have discovered. Along these lines, it is even more remarkable that the universe and its phenomena can be described using mathematical relationships, which reflects an underlying rationale to the universe itself.

    For most of the history of science, the discovery and exploration of the mathematical nature of the universe has been confined to physics and, to a lesser extent, chemistry. Because of the complexity and diversity of biological systems, many people working in the life sciences have questioned if simple mathematical rules exist in biology and could ever be discovered.

    But the discovery of a simple rule that predicts the behavior of mutualistic relationships in ecosystems suggests that mathematical relationships do describe and govern biological phenomena. And, as the researchers point out, their discovery may turn out to be the rule rather than the exception.

    From my perspective, a universe governed by mathematical relationships suggests that a deep, underlying rationale undergirds nature, which is precisely what I would expect if a Mind was behind the universe. To put it differently, if a Creator was responsible for the universe, as a Christian, I would expect that mathematical relationships would define the universe’s structure and function. In like manner, if the origin and design of living systems originated from a Creator, it would make sense that biological systems would possess an underlying mathematical structure as well—though it might be hard for us to discern these relationships because of the systems’ complexity.

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    Figure: The Mathematical Universe. Image credit: Shutterstock.

    The mathematical structure of the universe—and maybe even of biology—makes the world around us intelligible. And intelligibility is precisely what we would expect if the universe and everything in it were the products of a Creator—one who desired to make himself known to us through the creation (Romans 1:20). It is also what we would expect if human beings were made in God’s image (as Scripture describes), with the capacity to discern God’s handiwork in the world around us.

    A Case against Materialism

    But what if humans—including our minds—were cobbled together by evolutionary processes? Why would we expect human beings to be capable of making sense of the world around us? For that matter, why would we expect the universe—including the biological realm—to adhere to mathematical relationships?

    In other words, the mathematical undergirding of nature fits better in a theistic conception of reality than one rooted in materialism. And toward that end, the discovery by the Duke University investigators points to God’s role in the origin and design of life.

    Is There a Biological Anthropic Principle?

    As the Duke University scientists show, the discovery of a simple mathematical relationship describing the behavior of mutualistic interactions in ecosystems suggests that these types of relationships may be more commonplace than most life scientists thought or imagined. (See Biochemical Anthropic Principle in the Resources section.)

    This discovery also suggests that a cornerstone feature of ecosystems—mutualistic relationships—is not the haphazard product of evolutionary history. Instead, scientists observe a process fundamentally dictated and constrained by the laws of nature as revealed in the simple mathematical rule that describes the behavior of these systems. We can infer that mutualism within ecosystems may not be the outworking of chance events—the consequence of a historically contingent evolutionary process. Rather, these relationships appear to be fundamentally prescribed by the design of the universe. In other words, mutualism in ecosystems is inevitable in a universe like ours.

    For me, it is eerie to think that mutualism, which appears to be specified by the laws of nature, is precisely what is needed to maintain stable ecosystems. The universe appears to be structured in a just-right way so that stable ecosystems result. If the universe was any other way, then mutualism wouldn’t exist nor would ecosystems.

    One way to interpret this “coincidence” is to view it as evidence that our universe has been designed for a purpose. And purpose must come from a Mind—namely, God.

    Resources

    The Argument from Math and Beauty

    Designed for Discovery

    The Biochemical Anthropic Principle

    The Design of Intermediary Metabolism

    Endnotes
    1. Feilun Wu et al., “A Unifying Framework for Interpreting and Predicting Mutualistic Systems, Nature Communications 10 (2019): 242, doi:/10.1038/s41467-018-08188-5.
    2. Duke University, “Simple Rules Predict and Explain Biological Mutualism,” ScienceDaily (January 16, 2019), https://www.sciencedaily.com/releases/2019/01/190116110941.htm.
    3. Wu et al., “A Unifying Framework.”
  • ATP Transport Challenges the Evolutionary Origin of Mitochondria

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | Aug 21, 2019

    In high school, I spent most Sunday mornings with my family gathered around the TV watching weekly reruns of the old Abbott and Costello movies.

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    Image: Bud Abbott and Lou Costello. Image credit: Wikipedia

    One of my favorite routines has the two comedians trying to help a woman get her parallel-parked car out of a tight parking spot. As Costello takes his place behind the wheel, Abbott tells him to “Go ahead and back up.” And of course, confusion and hilarity follow as Costello repeatedly tries to clarify if he is to “go ahead” or “back up,” finally yelling, “Will you please make up your mind!”

    As it turns out, biologists who are trying to account for the origin of mitochondria (through an evolutionary route) are just as confused about directions as Costello. Specifically, they are trying to determine which direction ATP transport occurred in the evolutionary precursors to mitochondria (referred to as pre-mitochondria).

    In an attempt to address this question, a research team from the University of Virginia (UVA) has added to the frustration, raising new challenges for evolutionary explanations for the origin of mitochondria. Their work threatens to drive the scientific community off the evolutionary route into the ditch when it comes to explaining the origin of eukaryotic cells.1

    To fully appreciate the problems this work creates for the endosymbiont hypothesis, a little background is in order. (For those familiar with the evidence for the endosymbiont hypothesis, you may want to skip ahead to The Role of Mitochondria.)

    The Endosymbiont Hypothesis

    Most biologists believe that the endosymbiont hypothesis serves as the best explanation for the origin of complex cells.

    According to this idea, complex cells originated when symbiotic relationships formed among single-celled microbes after free-living bacterial and/or archaeal cells were engulfed by a “host” microbe.

    The “poster children” of the endosymbiont hypothesis are mitochondria. Presumably, the mitochondria started its evolutionary journey as an endosymbiont. Evolutionary biologists believe that once engulfed by the host cell, this microbe took up permanent residency, growing and dividing inside the host. Over time, the endosymbiont and the host became mutually interdependent, with the endosymbiont providing a metabolic benefit for the host cell (such as providing a source of ATP). In turn, the host cell provided nutrients to the endosymbiont. Presumably, the endosymbiont gradually evolved into an organelle through a process referred to as genome reduction. This reduction resulted when genes from the endosymbiont’s genome were transferred into the genome of the host organism, generating the mitonuclear genome.

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    Image: Endosymbiont Hypothesis. Image credit: Wikipedia

    Evidence for the Endosymbiont Hypothesis

    Much of the evidence for the endosymbiotic origin of mitochondria centers around the similarity between mitochondria and bacteria. These organelles are about the same size and shape as typical bacteria and have a double membrane structure like gram-negative cells. These organelles also divide in a way that is reminiscent of bacterial cells.

    Biochemical evidence also exists for the endosymbiont hypothesis. Evolutionary biologists view the presence of the diminutive mitochondrial genome as a vestige of this organelle’s evolutionary history. They see the biochemical similarities between mitochondrial and bacterial genomes as further evidence for the evolutionary origin of these organelles.

    The presence of the unique lipid, cardiolipin, in the mitochondrial inner membrane also serves as evidence for the endosymbiont hypothesis. This important lipid component of bacterial inner membranes is absent in the membranes of eukaryotic cells—except for the inner membranes of mitochondria. In fact, biochemists consider cardiolipin a signature lipid for mitochondria and a vestige of the organelle’s evolutionary history.

    The Role of Mitochondria

    Mitochondria serve cells in a number of ways, including:

    • Calcium storage
    • Calcium signaling
    • Signaling with reactive oxygen species
    • Regulation of cellular metabolism
    • Heat production
    • Apoptosis

    Arguably one of the most important functions of mitochondria relates to their role in energy conversion. This organelle generates ATP molecules by processing the breakdown products of glycolysis through the tricarboxylic acid cycle and the electron transport chain.

    Biochemists refer to ATP as a high-energy compound—it serves as an energy currency for the cell, and most cellular processes are powered by ATP. One way that ATP provides energy is through its conversion to ADP and an inorganic phosphate molecule. This breakdown reaction liberates energy that can be coupled to cellular activities that require energy.

     

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    Image: The ATP/ADP Reaction Cycle. Image credit: Shutterstock

    ATP Production and Transport

    The enzyme complex ATP synthase, located in the mitochondrial inner membrane, generates ATP from ADP and inorganic phosphate, using a proton gradient generated by the flow of electrons through the electron transport chain. As ATP synthase generates ATP, it deposits this molecule in the innermost region of the mitochondria (called the matrix or the lumen).

    In order for ATP to become available to power cellular processes, it has to be transported out of the lumen and across the mitochondrial inner membrane into the cytoplasm. Unfortunately, the inner mitochondrial membrane is impermeable to ATP (and ADP). In order to overcome this barrier, a protein embedded in the inner membrane called ATP/ADP translocase performs the transport operation. Conveniently, for every molecule of ATP transported out of the lumen, a molecule of ADP is transported from the cytoplasm into the lumen. In turn, this ADP is converted into ATP by ATP synthase.

    Because of the importance of this process, copies of ATP/ADP translocase comprises 10% of the proteins in the inner membrane.

    If this enzyme doesn’t function properly, it will result in mitochondrial myopathies.

    The Problem ATP Transport Causes for The Endosymbiont Hypothesis

    Two intertwined questions confronting the endosymbiont hypothesis relate to the evolutionary driving force behind symbiogenesis and the nature of pre-mitochondria.

    Traditionally, evolutionary biologists have posited that the host cell was an anaerobe, while the endosymbiont was an aerobic microbe, producing ATP from lactic acid generated by the host cell. (Lactic acid is the breakdown product of glucose in the absence of oxygen).

    But, as cell biologist Franklin Harold points out, this scenario has an inherent flaw. Namely, if the endosymbiont is producing ATP necessary for its survival from host cell nutrients, why would it relinquish some—or even all—of the ATP it produces to the host cell?

    According to Harold, “The trouble is that unless the invaders share their bounty with the host, they will quickly outgrow him; they would be pathogens, not symbionts.”2

    And, the only way they could share their bounty with the host cell is to transport ATP from the engulfed cell’s interior to the host cell’s cytoplasm. While mitochondria accomplish this task with the ATP/ADP translocase, there is no good reason to think that the engulfed cell would do this. Given the role ATP plays as the energy currency in the cell and the energy that is expended to make this molecule, there is no advantage for the engulfed cell to pump ATP from its interior to the exterior environment.

    Harold sums up the problem this way: “Such a carrier would not have been present in the free-living symbiont but must have been acquired in the course of its enslavement; it cannot be called upon to explain the initial benefits of the association.”3

    In other words, currently, there is no evolutionary explanation for why the ATP/ADP translocase in the mitochondrial inner membrane—a protein central to the role of mitochondria in eukaryotic cells—pumps ATP from the lumen to the cytoplasm.

    Two Alternative Models

    This problem has led evolutionary biologists to propose two alternative models to account for the evolutionary driving force behind symbiogenesis: 1) the hydrogen hypothesis; and 2) the oxygen scavenger hypothesis.

    The hydrogen hypothesis argues that the host cell was a methanogenic member of archaea that consumed hydrogen gas and the symbiont was a hydrogen-generating alpha proteobacteria.

    The oxygen-scavenging model suggests that the engulfed cell was aerobic, and because it used oxygen, it reduced the amount of oxygen in the cytoplasm of the host cell, thought to be an anaerobe.

    Today, most evolutionary biologists prefer the hydrogen hypothesis—in part because the oxygen scavenger model, too, has a fatal flaw. As Harold points out, “This [oxygen scavenger model], too, is dubious, because respiration generates free radicals that are known to be a major source of damage to cellular membranes and genes.”4

    Moving Forward, Or Moving Backward?

    To help make headway, two researchers from UVA attempted to reconstruct the evolutionary precursor to mitochondria, dubbed pre-mitochondria.

    Operating within the evolutionary framework, these two investigators reconstructed the putative genome of pre-mitochondria using genes in the mitochondrial genome and genes from the nuclear genomes of organisms they believe were transferred to the nucleus during the process of symbiogenesis. (Genes that clustered with alphaproteobacterial genes were deemed to be of mitochondrial origin.)

    Based on their reconstruction, they conclude that the original engulfed cell actually used its ATP/ADP translocase to import ATP from the host cell cytoplasm into its interior, exchanging the ATP for an ADP. This is the type of ATP/ADP translocase found in obligate intracellular parasites alive today.

    According to the authors, this means that:

    “Pre-mitochondrion [was] an ‘energy scavenger’ and suggests an energy parasitism between the endosymbiont and its host at the origin of the mitochondria. . . . This is in sharp contrast with the current role of mitochondria as the cell’s energy producer and contradicts the traditional endosymbiotic theory that the symbiosis was driven by the symbiont supplying the host ATP.5

    The authors speculate that at some point during symbiogenesis the ATP/ADP translocase went ahead and backed up, reversing direction. But, this explanation is little more than a just-so story with no evidential support. Confounding their conjecture is their discovery that the ATP/ADP translocase found in mitochondria is evolutionarily unrelated to the ATP/ADP translocases found in obligate intracellular parasites.

    The fact that the engulfed cell was an obligate intracellular parasite not only brings a halt to the traditional version of the endosymbiont hypothesis, it flattens the tires of both the oxygen scavenger model and hydrogen hypothesis. According to Wang and Wu (the UVA investigators):

    “Our results suggest that mitochondria most likely originated from an obligate intracellular parasite and not from a free-living bacterium. This has important implications for our understanding of the origin of mitochondria. It implies that at the beginning of the endosymbiosis, the bacterial symbiont provided no benefits whatsoever to the host. Therefore we argue that the benefits proposed by various hypotheses (e.g, oxygen scavenger and hydrogen hypotheses) are irrelevant in explaining the establishment of the initial symbiosis.”6

    If the results of the analysis by the UVA researchers stand, it leaves evolutionary biologists with no clear direction when it comes to determining the evolutionary driving force behind the early stages of symbiogenesis or the evolutionary route to mitochondria.

    It seems that the more evolutionary biologists probe the question of mitochondrial origins, the more confusion and uncertainty results. In fact, there is not a coherent compelling evolutionary explanation for the origin of eukaryotic cells—one of the key events in life’s history. The study by the UVA investigators (along with other studies) casts aspersions on the most prominent evolutionary explanations for the origin of eukaryotes, justifying skepticism about the grand claim of the evolutionary paradigm: namely, that the origin, design, and history of life can be explained exclusively through evolutionary processes.

    In light of this uncertainty, can the origin of mitochondria, and hence eukaryotic cells, be better explained by a creation model? I think so, but for many scientists this is a road less traveled.

    Resources

    Challenges to the Endosymbiont Hypothesis:

    In Support of a Creation Model for the Origin of Eukaryotic Cells:

    ATP Production and the Case for a Creator:

    Endnotes
    1. Zhang Wang and Martin Wu, “Phylogenomic Reconstruction Indicates Mitochondrial Ancestor Was an Energy Parasite,” PLOS One 9, no. 10 (October 15, 2014): e110685, doi:10.1371/journal.pone.0110685.
    2. Franklin M. Harold, In Search of Cell History: The Evolution of Life’s Building Blocks (Chicago, IL: The University of Chicago Press, 2014), 131.
    3. Harold, In Search of Cell History, 131.
    4. Harold, In Search of Cell History, 132.
    5. Wang and Wu, “Phylogenomic Reconstruction.
    6. Wang and Wu, “Phylogenomic Reconstruction.
  • Does Information Come from a Mind?

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | Aug 14, 2019

    Imagine youre flying over the desert, and you notice a pile of rocks down below. Most likely, you would think little of it. But suppose the rocks were arranged to spell out a message. I bet you would conclude that someone had arranged those rocks to communicate something to you and others who might happen to fly over the desert.

    You reach that conclusion because experience has taught you that messages come from persons/people—or, rather, that information comes from a mind. And, toward that end, information serves as a marker for the work of intelligent agency.

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    Image credit: Shutterstock

    Recently, a skeptic challenged me on this point, arguing that we can identify numerous examples of natural systems that harbor information, but that the information in these systems arose through natural processes—not a mind.

    So, does information truly come from a mind? And can this claim be used to make a case for a Creator’s existence and role in life’s origin and design?

    I think it can. And my reasons are outlined below.

    Information and the Case for a Creator

    In light of the (presumed) relationship between information and minds, I find it provocative that biochemical systems are information systems.

    Two of the most important classes of information-harboring molecules are nucleic acids (DNA and RNA) and proteins. In both cases, the information content of these molecules arises from the nucleotide and amino acid sequences, respectively, that make up these two types of biomolecules.

    The information harbored in nucleotide sequences of nucleic acids and amino acid sequences of proteins is digital information. Digital information is represented by a succession of discrete units, just like the ones and zeroes that encode the information manipulated by electronic devices. In this respect, sequences of nucleotides and amino acids for discrete informational units that encode the information in DNA and RNA and proteins, respectively.

    But the information in nucleic acids and proteins also has analog characteristics. Analog information varies in an uninterrupted continuous manner, like radio waves used for broadcasting purposes. Analog information in nucleic acids and proteins are expressed through the three-dimensional structures adopted by both classes of biomolecules. (For more on the nature of biochemical information, see Resources.)

    If our experience teaches us that information comes from minds, then the fact that key classes of biomolecules are comprised of both digital and analog information makes it reasonable to conclude that life itself stems from the work of a Mind.

    Is Biochemical Information Really Information?

    Skeptics, such as philosopher Massimo Pigliucci, often dismiss this particular design argument, maintaining that biochemical information is not genuine information. Instead, they maintain that when scientists refer to biomolecules as harboring information, they are employing an illustrative analogy—a scientific metaphor—and nothing more. They accuse creationists and intelligent design proponents of misconstruing scientists use of analogical language to make the case for a Creator.1

    In light of this criticism, it is worth noting that the case for a Creator doesn’t merely rest on the presence of digital and analog information in biomolecules, but gains added support from work in information theory and bioinformatics.

    For example, information theorist Bernd-Olaf Küppers points out in his classic work Information and the Origin of Life that the structure of the information housed in nucleic acids and proteins closely resembles the hierarchical organization of human language.2 This is what Küppers writes:

    The analogy between human language and the molecular genetic language is quite strict. . . . Thus, central problems of the origin of biological information can adequately be illustrated by examples from human language without the sacrifice of exactitude.3

    Added to this insight is the work by a team from NIH who discovered that the information content of proteins bears the same mathematical structure as human language. To this end, they discovered that a universal grammar exists that defines the structure of the biochemical information in proteins. (For more details on the NIH teams work, see Resources.)

    In other words, the discovery that the biochemical information shares the same features as human language deepens the analogy between biochemical information and the type of information we create as human designers. And, in doing so, it strengthens the case for a Creator.

    Further Studies that Strengthen the Case for a Creator

    So, too, does other work, such as studies in DNA barcoding. Biologists have been able to identify, catalog, and monitor animal and plant species using relatively short, standardized segments of DNA within genomes. They refer to these sequences as DNA barcodes that are analogous to the barcodes merchants use to price products and monitor inventory.

    Typically, barcodes harbor information in the form of parallel dark lines on a white background, creating areas of high and low reflectance that can be read by a scanner and interpreted as binary numbers. Barcoding with DNA is possible because this biomolecule, at its essence, is an information-based system. To put it another way, this work demonstrates that the information in DNA is not metaphorical, but is in fact informational. (For more details on DNA barcoding, see DNA Barcodes Used to Inventory Plant Biodiversity in Resources.)

    Work in nanotechnology also strengthens the analogy between biochemical information and the information we create as human designers. For example, a number of researchers are exploring DNA as a data storage medium. Again, this work demonstrates that biochemical information is information. (For details on DNA as a data storage medium, see Resources.)

    Finally, researchers have learned that the protein machines that operate on DNA during processes such as transcription, replication, and repair literally operate like a computer system. In fact, the similarity is so strong that this insight has spawned a new area of nanotechnology called DNA computing. In other words, the cell’s machinery manipulates information in the same way human designers manipulate digital information. For more details, take a look at the article “Biochemical Turing Machines ‘Reboot’ the Watchmaker Argument” in Resources.)

    The bottom line is this: The more we learn about the architecture and manipulation of biochemical information, the stronger the analogy becomes.

    Does Information Come from a Mind?

    Other skeptics challenge this argument in a different way. They assert that information can originate without a mind. For example, a skeptic recently challenged me this way:

    “A volcano can generate information in the rocks it produces. From [the] information we observe, we can work out what it means. Namely, in this example, that the rock came from the volcano. There was no Mind in information generation, but rather minds at work, generating meaning.

    Likewise, a growing tree can generate information through its rings. Humans can also generate information by producing sound waves.

    However, I dont think that volcanoes have minds, nor do trees—at least not the way we have minds.”

    –Roland W. via Facebook

    I find this to be an interesting point. But, I don’t think this objection undermines the case for a Creator. Ironically, I think it makes the case stronger. Before I explain why, though, I need to bring up an important clarification.

    In Roland’s examples, he conflates two different types of information. When I refer to the analogy between human languages and biochemical information, I am specifically referring to semantic information, which consists of combinations of symbols that communicate meaning. In fact, Roland’s point about humans generating information with sound waves is an example of semantic information, with the sounds serving as combinations of ephemeral symbols.

    The type of information found in volcanic rocks and tree rings is different from the semantic information found in human languages. It is actually algorithmic information, meaning that it consists of a set of instructions. And technically, the rocks and tree rings dont contain this information—they result from it.

    The reason why we can extract meaning and insight from rocks and tree rings is because of the laws of nature, which correspond to algorithmic information. We can think of these laws as instructions that determine the way the world works. Because we have discovered these laws, and because we have also discovered nature’s algorithms, we can extract insight and meaning from studying rocks and tree rings.

    In fact, Küppers points out that biochemical systems also consist of sets of instructions instantiated within the biomolecules themselves. These instructions direct activities of the biomolecular systems and, hence, the cell’s operations. To put it another way, biochemical information is also algorithmic information.

    From an algorithmic standpoint, the information content relates to the complexity of the instructions. The more complex the instructions, the greater the information content. To illustrate, consider a DNA sequence that consists of alternating nucleotides, AGAGAGAG . . . and so on. The instructions needed to generate this sequence are:

    1. Add an A
    2. Add a G
    3. Repeat steps 1 and 2, x number of times, where x corresponds to the length of the DNA sequence divided by 2

    But what about a DNA sequence that corresponds to a typical gene? In effect, because there is no pattern to that sequence, the set of instructions needed to create that sequence is the sequence itself. In other words, a much greater amount of algorithmic information resides in a gene than in a repetitive DNA sequence.

    And, of course, our common experience teaches us that information—whether it’s found in a gene, a rock pile, or a tree ring—comes from a Mind.

    Resources

    Endnotes
    1. For example, see Massimo Pigliucci and Maarten Boudry, “Why Machine-Information Metaphors Are Bad for Science and Science Education,” Science and Education 20, no. 5–6 (May 2011): 453–71; doi:10.1007/s11191-010-9267-6.
    2. Bernd-Olaf Küppers, Information and the Origin of Life (Boston, MA: MIT Press, 1990), 24–25.
    3. Küppers, Information, 23.
  • New Insights into Endothermy Heat Up the Case for a Creator

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | Aug 07, 2019

    I feel cold all the time.

    When I was younger, I was always hot. I needed to be in air conditioning everywhere I went. I could never get the temperature cold enough. But now that I am older, I feel like a frail person who is always chilled, needing to drape myself with a blanket to keep warm.

    Nevertheless, like all human beings, I am still warm-blooded. I am an endotherm, as are all mammals and birds.

    For many biologists, endothermy represents a bit of an enigma. Maintaining a constant body temperature requires an elevated basal metabolic rate. But the energy needed to preserve a constant body temperature doesn’t come cheap. In fact, warm-blooded animals demand 30 times the energy per unit time compared to cold-blooded (ectothermic) creatures.

    Though biologists have tried to account for endothermy, no model has adequately explained why birds and mammals are warm-blooded. The advantages of being warm-blooded over being cold-blooded have not seemed to adequately outweigh costs—until now.

    Recently, a biologist from the University of Nevada, Reno, Michael L. Logan, published a model that helps make sense of this enigma.1 His work evokes the optimal design and elegant rationale for endothermy in birds and mammals—and ectothermy in amphibians and reptiles.

    An Explanation for Endothermy

    For endothermy to exist, it must confer some significant advantage for animals constant, elevated body temperatures.

    Logan argues that endothermy maintains mammalian and bird body temperatures close to the thermal optimum for immune system functionality. The operations of the immune system are temperature-dependent. If the temperature is too low or too high, the immune system responds poorly to infectious agents. But an elevated and stable body temperature primes mammalian and bird immune systems to rapidly and effectively respond to pathogens. When birds and mammals acquire a pathogen, their bodies mount a fever response. This slight elevation in temperature places their body temperature at the thermal optimum.

    In other words, the fever response plays a critical role when animals battle infectious agents. And warm-blooded animals have the advantage of possessing body temperatures close to ideal.

    Temperature and Immune System Function

    A body of evidence indicates that the immune systems components display temperature-dependent changes in activity. As it turns out, fever optimizes immune system function by:

    1. Increasing the flow of blood through the bloodstream because of the vasodilation (blood vessel expansion) associated with fever. This increased blood flow accelerates the movement of immune cells throughout the body, giving them more timely access to pathogens.
    2. Increasing binding of immune system proteins to immune cells, assisting their trafficking to lymph tissue.
    3. Increasing cellular activity, such as proliferation and differentiation of immune cells and phagocytosis.

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    Figure: The Human Immune System. Image credit: Shutterstock

    Other studies indicate that some pathogens, such as fungi, lose virulence at higher temperatures, further accounting for elevated body temperatures and the importance of the fever response. Of course, if body temperature becomes too high, it will compromise immune system function, moving it away from the temperature optimum and leading to other complications. So, the fever response must be carefully regulated.

    Heres the key point: the metabolic costs of endothermy are justified because warm-bloodedness allows the immune systems of birds and mammals to be near enough to the temperature optimum that infectious agents can be quickly cleared from their bodies.

    Fever Response in Ectotherms

    Cold-blooded animals (ectotherms) also mount a fever response to infectious agents for the same reason as endotherms. However, the body temperature of ectotherms is set by their surroundings. This limitation means that ectotherms need to regulate their body temperature and mount the fever response through their behavior by moving into spaces with elevated temperatures. Doing so places them at the mercy of environmental changes. This condition means that cold-blooded creatures experience a significant time lag between the onset of infection and the fever response. It also means that, in some cases, ectotherms can’t elevate their body temperature to the immune system optimum if, for example, it is night or overcast.

    Finally, in an attempt to elevate their body temperatures, ectotherms need to be out from under cover, making themselves vulnerable to predators. So, according to Logan’s model, endothermy offers some tangible advantages compared to ectothermy.

    But endothermy comes at a cost. As mentioned, the metabolic cost of endothermy is extensive compared to ectothermy. Pathogen virulence marks another disadvantage. Logan points out that pathogens that infect cold-blooded animals are much less virulent than pathogens that infect warm-blooded creatures.

    Endothermy and Ectothermy Trade-Offs

    So, when it comes to regulation of animal body temperature, a set of trade-offs exists that include:

    • Metabolic costs
    • Immune system responsiveness and effectiveness
    • Pathogen virulence
    • Vulnerability to predators

    These trade-offs can be managed by two viable strategies: endothermy and ectothermy. Each has advantages and disadvantages. And each is optimized in its own right.

    Regulation of Body Temperature and the Case for a Creator

    Logan seeks to account for the evolutionary origins of endothermy by appealing to the advantages it offers organisms battling pathogens. But, examining Logans scenario leaves one feeling as if the explanation is little more than an evolutionary just-so story.

    When endothermy presented an enigma for biologists, it would have been hard to argue that it reflected the handiwork of a Creator, particularly in light of its large metabolic cost. But now that scientists understand the trade-offs in play and the optimization associated with the endothermic lifestyle, we can also interpret the optimization of endothermy and ectothermy as evidence for design.

    From my vantage point, optimization signifies the handiwork of a Creator. As I discuss in The Cell’s Design, saying something is optimized is equivalent to saying it is well-designed. The optimization of an engineered system doesn’t just happen. Rather, such systems require forethought, planning, and careful attention to detail. In the same way, the optimized designs of biological systems like endothermy and ectothermy reasonably point to the work of a Creator.

    And I am chill with that.

    Resources

    Endnotes
    1. Michael L. Logan, “Did Pathogens Facilitate the Rise of Endothermy?” Ideas in Ecology and Evolution 12 (June 4, 2019): 1–8, https://ojs.library.queensu.ca/index.php/IEE/article/view/13342.
  • Is SETI an Intelligent Design Research Program?

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | Jul 24, 2019

    When I was a little kid, my father was chair of the physics department at West Virginia Institute of Technology (WVIT). We lived in faculty housing on the outskirts of the WVIT campus and, as a result, the college grounds became my playground.

    I have always felt at home on college and university campuses. Perhaps this is one reason I enjoy speaking at university venues. I also love any chance I get to interact with college students. They have inquisitive minds and they won’t hesitate to challenge ideas.

    Skeptical Challenge

    A few years ago I was invited to present a case for a Creator, using evidence from biochemistry, at Cal Poly San Luis Obispo. During the Q&A session, a skeptical student challenged my claims, insisting that intelligent design/creationism isn’t science. In leveling this charge, he was advocating scientism—the view that science is the only way to discover truth; in fact, science equates to truth. Thus, if something isn’t scientific, then it can’t be true. On this basis he rejected my claims.

    You might be surprised by my response. I agreed with my questioner.

    My case for a Creator based on the design of biochemical systems is not science. It is a philosophical and theological argument informed by scientific discovery. In other words, scientific discoveries have metaphysical implications. And, by identifying and articulating those implications, I built a case for God’s existence and role in the origin and design of life.

    Having said this, I do think that design detection is legitimately part of the fabric of science. We can use scientific methodologies to detect the work of intelligent agency. That is, we can develop rigorous scientific evidence for intelligent design. I also think we can ascribe attributes to the intelligent designer from scientific evidence at hand.

    In defense of this view, I (and others who are part of the Intelligent Design Movement, or IDM) have pointed out that there are branches of science that function as intelligent design programs, such as research in archaeology and the Search for Extraterrestrial Intelligence (SETI). We stand to learn much from these disciplines about the science of design detection. (For a detailed discussion, see the Resources section.)

    SETI and Intelligent Design

    Recently, I raised this point in a conversation with another skeptic. He challenged me on that point, noting that Seth Shostak, an astronomer from the SETI Institute, wrote a piece for Space.com repudiating the connection between intelligent design (ID) and SETI, arguing that they don’t equate.

     

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    Figure: Seth Shostak. Image credit: Wikipedia

    According to Shostak,

    “They [intelligent design proponents] point to SETI and say, ‘upon receiving a complex radio signal from space, SETI researchers will claim it as proof that intelligent life resides in the neighborhood of a distant star. Thus, isn’t their search completely analogous to our own line of reasoning—a clear case of complexity implying intelligence and deliberate design? And SETI, they would note, enjoys widespread scientific acceptance.”1

    Shostak goes on to say, “If we as SETI researchers admit this is so, it sounds as if were guilty of promoting a logical double standard. If the ID folks arent allowed to claim intelligent design when pointing to DNA, how can we hope to claim intelligent design on the basis of a complex radio signal?”2

    In an attempt to distinguish the SETI Institute from the IDM, Shostak asserts that ID proponents make their case for intelligent design based on the complexity of biological and biochemical systems. But this is not what the SETI Institute does. According to Shostak, “The signals actually sought by today’s SETI searches are not complex, as the ID advocates assume. We’re not looking for intricately coded messages, mathematical series, or even the aliens’ version of ‘I Love Lucy.’”

    Instead of employing complexity as an indicator of intelligent agency, SETI looks for signals that display the property of artificiality. What they mean by artificiality is that specifically, SETI is looking for a simple signal of narrow-band electromagnetic radiation that forms an endless sinusoidal pattern. According to SETI investigators, this type of signal does not occur naturally. Shostak also points out that the context of the signal is important. If the signal comes from a location in space that couldn’t conceivably harbor life, then SETI researchers would be less likely to conclude that it comes from an intelligent civilization. On the other hand, if the signal comes from a planetary system that appears life-friendly, this signal would be heralded as a successful detection event.

    Artificiality and Intelligent Design

    I agree with Shostak. Artificiality, not complexity, is the best indicator of intelligent design. And, it is also important to rule out natural process explanations. I can’t speak for all creationists and ID proponents, but the methodology I use to detect design in biological systems is precisely the same one the SETI Institute employs.

    In my book The Cell’s Design, I propose the use of an ID pattern to detect design. Toward this end, I point out that objects, devices, and systems designed by human beings—intelligent designers—are characterized by certain properties that are distinct from objects and systems generated by natural processes. To put it in Shostak’s terms, human designs display artificiality. And we can use the ID pattern as a way to define what artificiality should look like.

    Here are three ways I adopt this approach:

    1. In The Cell’s Design, I follow after natural theologian William Paley’s work. Paley described designs created by human beings as contrivances in which the concept of artificiality was embedded. I explain examples of such artificiality in biochemical systems.
    2. In Origins of Life (a work I coauthored with astronomer Hugh Ross) and Creating Life in the Lab, I point out that natural processes don’t seem to be able to account for the origin of life and, hence, the origin of biochemical systems.
    3. Finally, in Creating Life in the Lab, I show that attempts to create protocells starting with simple molecules and attempts to recapitulate the different stages in the origin-of-life pathway depend upon intelligent agency. This dependence further reinforces the artificiality displayed by biochemical systems.

    Collectively, all three books present a comprehensive case for a Creator’s role in the origin and fundamental design of life, with each component of the overall case for design resting on the artificiality of biochemical systems. So, even though the SETI Institute may want to distance themselves from the IDM, SETI is an intelligent design program. And intelligent design is, indeed, part of the construct of science.

    In other words, scientists from a creation model perspective can make a rigorous scientific case for the role of intelligent agency in the origin and design of biochemical systems, and even assign attributes to the designer. At that point, we can then draw metaphysical conclusions about who that designer might be.

    Resources

    Endnotes
    1. Seth Shostak, “SETI and Intelligent Design,” Space.com (December 1, 2005), https://www.space.com/1826-seti-intelligent-design.html.
    2. Shostak, “SETI and Intelligent Design.”
  • Does Old-Earth Creationism Make God Deceptive?

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | Jul 17, 2019

    “Are [vestigial structures] unequivocal evidence of evolution?

    No. Are they reasonable evidence of evolution? Yes.

    Ditto gene sequences.

    Appearance of evolution is no more a valid deflection [for the overwhelming evidence for evolution] than the appearance of age is a valid dodge of the overwhelming confluence of evidence of antiquity.

    Both are sinking ships. I got off before going under with you on this one.”

    —Hill R. (a former old-earth creationist who now espouses theistic evolution/evolutionary creationism)

    Most people who follow my work at Reasons to Believe know I question the grand claim of the evolutionary paradigm; namely, that evolutionary processes provide the exclusive explanation for the origin, design, and history of life. In light of my skepticism, friends and foes alike often ask me how I deal with (what many people perceive to be) the compelling evidence for the evolutionary history of life, such as vestigial structures and shared genetic features in genomes.

    As part of my response, I point out that this type of evidence for evolution can be accommodated by a creation model, with the shared features reflecting common design, not common descent—particularly now that we know that there is a biological rationale for many vestigial structures and shared genetic features. This response prompted my friend Hill R. to level his objection. In effect, Hill says I am committing the “appearance of evolution” fallacy, which he believes is analogous to the “appearance of age” fallacy committed by young-earth creationists (YECs).

    Hill is not alone in his criticism. Other people who embrace theistic evolution/evolutionary creation (such as my friends at BioLogos) level a similar charge. According to these critics, both appearance of age and appearance of evolution fallacies make God deceptive.

    If biological systems are designed, but God made them appear as if they evolved, then the conclusions we draw when we investigate nature are inherently untrustworthy. This is a problem because, according to Scripture, God reveals himself to us through the record of nature. But if we are misled by natures features and, consequently, draw the wrong conclusion, then it makes God deceptive. However, God cannot lie or deceive. It is contrary to his nature.

    So, how do I respond to this theological objection to RTB’s creation model?

    Before I reply, I want to offer a little more background information to make sure that anyone who is unfamiliar with this concern can better appreciate the seriousness of the charge against our creation model. If you don’t need the background explanation, then feel free to skip ahead to A Response to the Appearance of Evolution Challenge.

    Evidence for Evolution: Vestigial Structures

    Evolutionary biologists often point to vestigial structures—such as the pelvis and hind limbs of whales and dolphins (cetaceans)—as compelling evidence for biological evolution. Evolutionary biologists view vestigial structures this way because they are also homologous (structurally similar) structures. Vestigial structures are rudimentary body parts that are smaller and simpler than the corresponding features possessed by the other members of a biological group. As a case in point, the whale pelvis and hind limbs are homologous to the pelvis and hind limbs of all other mammals.

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    Figure 1: Whale Pelvis. Image credit: Shutterstock

    Evolutionary biologists believe that vestigial structures were fully functional at one time but degenerated over the course of many generations because the organisms no longer needed them to survive in an ever-changing environment—for example, when the whale ancestor transitioned from land to water. From an evolutionary standpoint, fully functional versions of these structures existed in the ancestral species. The structures’ form and function may be retained (possibly modified) in some of the evolutionary lineages derived from the ancestral species, but if no longer required, the structures become diminished (and even lost) in other lineages.

    Evidence for Evolution: Shared Genetic Features

    Evolutionary biologists also consider shared genetic features found in organisms that naturally group together as compelling evidence for common descent. One feature of particular interest is the identical (or nearly identical) DNA sequence patterns found in genomes. According to this line of reasoning, the shared patterns arose as a result of a series of substitution mutations that occurred in the common ancestor’s genome. Presumably, as the varying evolutionary lineages diverged from the nexus point, they carried with them the altered sequences created by the primordial mutations.

    Synonymous mutations play a significant role in this particular argument for common descent. Because synonymous mutations don’t alter the amino acid sequence of proteins, their effects are considered to be inconsequential. (In a sense, they are analogous to vestigial anatomical features.) So, when the same (or nearly the same) patterns of synonymous mutations are observed in genomes of organisms that cluster together into the same group, most life scientists interpret them as compelling evidence of the organisms’ common evolutionary history.

    A Response to the Evidence for Evolution

    As a rejoinder to this evidence, I point out that we continue to uncover evidence that vestigial structures display function (see Vestigial Structures are Functional in the Resources section.) Likewise, evidence is beginning to accumulate that synonymous mutations have functional consequences. (see Shared Genetic Features Reflect Design in the Resources section.) Again, if these features have functional utility, then they can reasonably be interpreted as the Creator’s handiwork.

    But, even though these biological features bear function, many critics of the RTB model think that the shared features of these biological systems still bear the hallmarks of an evolutionary history. Therefore, they argue that these features look as if they evolved. And if so, we are guilty of the “appearance of evolution fallacy.

    Appearance of Age and the Appearance of Evolution

    In 1857, Philip Gosse, a biologist and preacher from England, sought to reconcile the emerging evidence for Earth’s antiquity with Scripture. Gosse was convinced that the earth was old. He was also convinced that Scripture taught that the earth was young. In an attempt to harmonize these disparate stances, he proposed the appearance of age argument in a book titled Omphalos. In this work, Gosse argued that God created Earth in six days, but made it with the appearance of age.

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    Figure 2: Philip Henry Gosse, 1855. Image credit: Wikipedia

    This idea persists today, finding its way into responses modern-day YECs make to the scientific evidence for Earth’s and life’s antiquity. For many people (including me), the appearance of age argument is fraught with theological problems, the chief one being that it makes God deceptive. If Earth appears to be old, and it measures to be old, yet it is young, then we can’t trust anything we learn when we study nature. This problem is not merely epistemological; it is theological because nature is one way that God has chosen to make himself known to us. But if our investigation of nature is unreliable, then it means that God is untrustworthy.

    In other words, on the surface, both the appearance of age and the appearance of evolution arguments made by YECs and old-earth creationists (OECs), respectively, seem to be equally problematic.

    But does the RTB position actually commit the appearance of evolution fallacy? Does it suffer from the same theological problems as the argument first presented by Gosse in Omphalos? Are we being hypocritical when we criticize the appearance of age fallacy, only to commit the appearance of evolution fallacy?

    A Response to the Appearance of Evolution Challenge

    This charge against the RTB creation model neglects to fully represent the reasons I question the evolutionary paradigm.

    First, my skepticism is not theologically motivated but scientifically informed. For example, I point out in an article I recently wrote for Sapientia that a survey of the scientific literature makes it clear that evolutionary theory as currently formulated cannot account for the key transitions in life’s history, including:

    • the origin of life
    • the origin of eukaryotic cells
    • the origin of body plans
    • the origin of human exceptionalism

    Additionally, some predictions that flow out of the evolutionary paradigm have failed (such as the widespread prevalence of convergence), further justifying my skepticism. (See Scientific Challenges to the Evolutionary Paradigm in the Resources section.)

    In other words, when we interpret shared features as a manifestation of common design (including vestigial structures and shared genetic patterns), it is in the context of scientifically demonstrable limitations of the evolutionary framework to fully account for life’s origin, history, and design. To put it differently, because of the shortcomings of evolutionary theory, we don’t see biological systems as having evolved. Rather, we think they’ve been designed.

    Appearance of Design Fallacy

    Even biologists who are outspoken atheists readily admit that biological and biochemical systems appear to be designed. Why else would Nobel Laureate Francis Crick offer this word of caution to scientists studying biochemical systems: “Biologists must keep in mind that what they see was not designed, but rather evolved.”1 What other reason would evolutionary biologist Richard Dawkins offer for defining biology as “the study of complicated things that give the appearance of having been designed for a purpose”?2

    Biologists can’t escape the use of design language when they describe the architecture and operation of biological systems. In and of itself, this practice highlights the fact that biological systems appear to be designed, not evolved.

    To sidestep the inexorable theological implications that arise when biologists use design language, biologist Colin Pittendrigh coined the term teleonomy in 1958 to describe systems that appear to be purposeful and goal-directed, but aren’t. In contrast with teleology—which interprets purposefulness and goal-directedness as emanating from a Mind— teleonomy views design as the outworking of evolutionary processes. In other words, teleonomy allows biologists to utilize design language— when they describe biological systems—without even a tinge of guilt.

    In fact, the teleonomic interpretation of biological design resides at the heart of the Darwinian revolution. Charles Darwin claimed that natural selection could account for the design of biological systems. In doing so, he supplanted Mind with mechanism. He replaced teleology with teleonomy.

    Prior to Darwin, biology found its grounding in teleology. In fact, Sir Richard Owen—one of England’s premier biologists in the early 1800s—produced a sophisticated theoretical framework to account for shared biological features found in organisms that naturally cluster together (homologous structures). For Owen (and many biologists of his time) homologous structures were physical manifestations of an archetypal design that existed in the Creator’s mind.

    Thus, shared biological features—whether anatomical, physiological, biochemical, or genetic—can be properly viewed as evidence for common design, not common descent. In fact, when Darwin proposed his theory of evolution, he appropriated Owen’s concept of the archetype but then replaced it with a hypothetical common ancestor.

    Interestingly, Owen (and other like-minded biologists) found an explanation for vestigial structures like the pelvis and hind limb bones (found in whales and snakes) in the concept of the archetype. They regarded these structures as necessary to the architectural design of the organism. In short, a model that interprets shared biological characteristics from a design/creation model framework has historical precedence and is based on the obvious design displayed by biological systems.

    Given the historical precedence for interpreting the appearance of design in biology as bona fide design and the inescapable use of design language by biologists, it seems to me that RTBs critics commit the appearance of design fallacy when they (along with other biologists) claim that things in biology look designed, but they actually evolved.

    Theories Are Underdetermined by Data

    A final point. One of the frustrating aspects of scientific discovery relates to whats called the underdetermination thesis.3 Namely, two competing theories can explain the same set of data. According to this idea, theories are underdetermined by data. This limitation means that two or more theories—that may be radically different from one another—can equally account for the same data. Or, to put it another way, the methodology of science never leads to one unique theory. Because of this shortcoming, other factors—nonscientific ones—influence the acceptance or rejection of a scientific theory, such as a commitment to mechanistic explanations to explain all of biology.

    As a consequence of the underdetermination theory, evolutionary models don’t have the market cornered when it comes to offering an interpretation of biological data. Creation models, such as the RTB model—which relies on the concept of common design—also makes sense of the biological data. And given the inability of current evolutionary theory to explain key transitions in life’s history, maybe a creation model approach is the better alternative.

    In other words, when we interpret vestigial structures and shared genetic features from a creation model perspective, we are not committing an appearance of age type of fallacy, nor are we making God deceptive. Instead, we are offering a common sense and scientifically robust interpretation of the elegant designs so prevalent throughout the living realm.

    Far from a sinking ship one should abandon, a creation model offers a lifeline to scientific and biblical integrity.

    Resources

    Vestigial Structures Are Functional

    Shared Genetic Features Reflect Design

    Scientific Challenges for the Evolutionary Paradigm

    Archetype Biology

    Endnotes
    1. Francis Crick, What Mad Pursuit: A Personal View of Scientific Discovery (New York: Basic Books, 1988), 138.
    2. Richard Dawkins, The Blind Watchmaker: Why the Evidence for Evolution Reveals a Universe without Design (New York: W. W. Norton, 1996), 4.
    3. Val Dusek, Philosophy of Technology: An Introduction (Malden, MA: Blackwell Publishing, 2006), 12.
  • Membrane Biochemistry Challenges Route to Evolutionary Origin of Complex Cells

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | Jul 10, 2019

    If you find yourself in need of directions when traveling through New England and you ask a local for help, he or she just might reply, “You can’t get there from here.” As you can imagine, these aren’t welcome words, particularly when all you want to do is make your way to your destination.

    Unfortunately, the same thing could be said to biologists trying to discover the evolutionary route that led to the emergence of complex, eukaryotic cells. No matter the starting point, it seems as if you just can’t get there from here.

    This frustration becomes most evident as evolutionary biologists try to account for the biochemical makeup of the membranes found in eukaryotic cells. In my opinion, this struggle is not just an inconvenient detour. As the following paragraphs show, obstacles line the roadway, ultimately leading to a dead end that exposes the shortcomings of the endosymbiont hypothesis—a cornerstone idea in evolutionary biology.

    Endosymbiont Hypothesis

    Most biologists believe that the endosymbiont hypothesis stands as the best explanation for the origin of complex cells. According to this hypothesis, complex cells originated when symbiotic relationships formed among single-celled microbes after free-living bacterial and/or archaeal cells were engulfed by a “host” microbe.

    The mitochondrion represents the “poster child” of the endosymbiont hypothesis. Presumably, this organelle started as an endosymbiont. Evolutionary biologists believe that once engulfed by the host cell, the microbe took up permanent residency, growing and dividing inside the host. Over time, the endosymbiont and host became mutually interdependent, with the endosymbiont providing a metabolic benefit—such as a source of ATP—for the host cell. In turn, the host cell provided nutrients to the endosymbiont. Presumably, the endosymbiont gradually evolved into an organelle through a process referred to as genome reduction. This reduction resulted when genes from the endosymbiont’s genome were transferred into the genome of the host organism.

    Evidence for the Endosymbiont Hypothesis
    1. Most of the evidence for the endosymbiont hypothesis centers around mitochondria and their similarity to bacteria. Mitochondria are about the same size and shape as a typical bacterium and have a double membrane structure like gram-negative cells. These organelles also divide in a way that is reminiscent of bacterial cells.

    2. Biochemical evidence also exists for the endosymbiont hypothesis. Evolutionary biologists view the presence of the diminutive mitochondrial genome as a vestige of this organelle’s evolutionary history. They see the biochemical similarities between mitochondrial and bacterial genomes as further evidence for the evolutionary origin of these organelles.

    3. The presence of the unique lipid, cardiolipin, in the mitochondrial inner membrane also serves as evidence for the endosymbiont hypothesis. This important lipid component of bacterial inner membranes is not found in the membranes of eukaryotic cells—except for the inner membranes of mitochondria. In fact, biochemists consider it a signature lipid for mitochondria and a vestige of the organelle’s evolutionary history. So far, the evolutionary route looks well-paved and clear.

    Discovery of Lokiarchaeota

    Evolutionary biologists have also developed other lines of evidence in support of the endosymbiont hypothesis. For example, biochemists have discovered that the genetic core (DNA replication and the transcription and translation of genetic information) of eukaryotic cells resembles that of the archaea. This similarity suggests to many biologists that a microbe belonging to the archaeal domain served as the host cell that gave rise to eukaryotic cells.

    Life scientists think they may have determined the identity of that archaeal host. In 2015, a large international team of collaborators reported the discovery of Lokiarchaeota, a new phylum belonging to the archaea. This phylum clusters with eukaryotes on the evolutionary tree. Analysis of the genomes of Lokiarchaeota identifies a number of genes involved in membrane-related activities, suggesting that this microbe may well have possessed the ability to engulf other microbes.1 At this point, it looks like you can get there from here.

    Challenges to the Endosymbiont Hypothesis

    Despite this seemingly compelling evidence, the evolutionary route to the first eukaryotic cells is littered with potholes. I have written several articles detailing some of the obstacles. (See Challenges to the Endosymbiont Hypothesis in the Resources section.) Also, a divide on the evolutionary roadway called the lipid divide compounds the problem for the endosymbiont hypothesis.

    Lipid Divide

    The lipid divide refers to the difference in the chemical composition of the cell membranes found in bacteria and archaea. Phospholipids comprise the cell membranes of both sorts of microbes. But the similarity ends there. The chemical makeup of the phospholipids is distinct in bacteria and archaea.

    Bacterial phospholipids are built around a d-glycerol backbone, which has a phosphate moiety bound to the glycerol in the sn-3 position. Two fatty acids are bound to the d-glycerol backbone at the sn-1 and sn-2 positions. In water, these phospholipids assemble into bilayer structures.

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    Figure: Difference between archaeal (top) and bacterial (middle and bottom) phospholipids. Features include 1: isoprene chains, 2: ether linkage, 3: l-glycerol, 4 and 8: phosphate group, 5: fatty acid chains, 6: ester linkages, 7: d-glycerol, 9: lipid bilayer of bacterial membranes, 10: lipid monolayer found in some archaea. Image credit: Wikipedia

    Archaeal phospholipids are constructed around an l-glycerol backbone (which produces membrane lipids with different stereochemistry than bacterial phospholipids). The phosphate moiety is attached to the sn-1 position of glycerol. Two isoprene chains are bound to the sn-2 and sn-3 positions of l-glycerol via ether linkages. Some archaeal membranes are formed from phospholipid bilayers, while others are formed from phospholipid monolayers.

    Presumably, the structural features of the archaeal phospholipids serve as an adaptation that renders them ideally suited to form stable membranes in the physically and chemically harsh environments in which many archaea find themselves.

    Lipid Divide Frustrates the Origin of Eukaryotic Cell Membranes

    In light of the lipid divide and the evidence that seemingly indicates that the endosymbiotic host cell likely belonged to Lokiarchaeota, it logically follows that the membrane composition of eukaryotic cells should be archaeal-like. But, this expectation is not met and the evolutionary route encounters another pothole. Instead, the cell membranes of eukaryotic cells closely resemble bacterial membranes.

    One way to repair the roadway is to posit that during the evolutionary process that led to the emergence of eukaryotic cells, a transition from archaeal-like membranes to bacterial-like membranes took place. In fact, supporting evidence comes from laboratory studies demonstrating that stable bilayers can form from a mixture of bacterial and archaeal phospholipids, even though the lipids from the two sources have opposite stereochemistry.

    Evolutionary biologists Purificación López-García and David Moreira question if evidence can be marshaled in support of this scenario for two reasons.2 First, mixing of phospholipids in the lab is a poor model for cell membranes that function as a “dynamic cell-environment interface.”3

    Second, they question if this transition is feasible given how exquisitely optimized membrane proteins must be to fit into cell membranes. The nature of protein optimization is radically different for bacterial and archaeal membranes. Because cell membrane systems are optimized, the researchers question if an adequate driving force for this transition exists.

    In other words, these two scientists express serious doubts about the biochemical viability of a transitional stage between archaeal membranes. In light of these obstacles, López-García and Moreira write, “The archaea-to-bacteria membrane shift remains the Achilles’ heel for these models [that propose an archaeal host for endosymbionts].”4

    In other words, you can’t get there from here.

    Can Lokiarchaeota Traverse the Lipid Divide?

    In the midst of this uncertain evolutionary route, a recent study by investigators from the Netherlands seems to point the way toward the evolutionary origin of eukaryotic membranes.5 Researchers screened the Lokiarchaeota genome for enzymes that would take part in phospholipid synthesis with the hope of finding clues about how this transition may have occurred. They conclude that this group of microbes could not make l-glycerol-1-phosphate (a key metabolic intermediate in the production of archaeal phospholipids) because it lacked the enzyme glycerol-1-phosphate dehydrogenase (G1PDH). They also discovered evidence that suggests that this group of microbes could make fatty acids and chemically attach them to sugars. The researchers argue that Lokiarchaeota could make some type of hybrid phospholipid with features of both archaeal and bacterial phospholipids.

    The team’s approach to understanding how evolutionary processes could bridge the lipid divide and account for the origin of eukaryotic membranes is clever and inventive, to be sure. But it is far from convincing for at least four reasons.

    1. Absence of evidence is not evidence of absence, as the old saying goes. Just because the research team didn’t find the gene for G1PDH in the Lokiarchaeota genetic material doesn’t mean this microbe didn’t have the capacity to make archaeal-type phospholipids. Toward this end, it is important to note that researchers have not cultured any microbe that belongs to this group organisms. The groups existence is inferred from metagenomic analysis, which involves isolating small fragments of DNA from the environment (in this case a hydrothermal vent system in the Atlantic Ocean, called Loki’s Castle) and stitching them together into a genome. The Lokiarchaeota “genome” is low quality (1.4-fold coverage) and incomplete (8 percent of the genome is missing). Around one-third (32 percent) of the genome codes for proteins with unknown function. Could it be that an enzyme capable of generating l-glycerol-1-phosphate exists in the mysterious third of the genome? Or in the missing 8 percent?

    2. While the researchers discovered that genes could conceivably work together to make d-glycerol-3-phosphate (though the enzymes encoded by these genes perform different metabolic functions), they found no direct evidence that Lokiarchaeota produces d-glycerol-3-phosphate. Nor did they find evidence for glycerol-3-phosphate dehydrogenase (G3PDH) in the Lokiarchaeota genetic material. This enzyme plays a key role in the synthesis of phospholipids in bacteria.

    3. Though the researchers found evidence that Lokiarchaeota had the capacity to make fatty acids, some of the genes required for the process seem to have been acquired by these microbes via horizontal gene transfer with genetic material from bacteria. (It should be noted that 29 percent of the Lokiarchaeota genome comes from the bacteria.) It is not clear when Lokiarchaeota acquired these genes and, therefore, if this metabolic capability has any bearing on the origin of eukaryotes.

    4. The researchers present no evidence that Lokiarchaeota possessed the protein machinery that would chemically attach isoprenoid lipids to d-glycerol-3-phosphate via ether linkages.

    Thus, the only way to establish Lokiarchaeota membranes as a transitional evolutionary pathway between those found in Archaea and Bacteria is to perform chemical analysis of its membranes. At this juncture, such analysis is impossible to perform because no one has been able to culture Lokiarchaeota. In fact, other evidence suggests that this group of microbes possessed archaeal-type membranes. Researchers have recovered archaeal lipids in the sediments surrounding Loki’s Castle, but they have not recovered bacterial-like lipids.

    More Lipid Divide Frustration

    Given these problems, could it be that the host microbe for the endosymbiont was a member of Bacteria, not Archaea? While this model would solve the problem of the lipid divide, it leaves unexplained the similarity between the genetic core of eukaryotes and the Archaea. Nor does it account for the grouping of eukaryotes with the Archaea.

    It doesn’t look like you can get there from here, either.

    Evolutionary biologists Jonathan Lombard, Purificación López-García and David Moreira sum things up when they write, “The origin of eukaryotic membranes is a problem that is rarely addressed by the different hypotheses that have been proposed to explain the emergence of eukaryotes.”6 Yet, until this problem is adequately addressed, the evolutionary route to eukaryotes will remain obscure and the endosymbiont hypothesis noncompelling.

    In light of this challenge and others, maybe a better way to make sense of the origin of eukaryotic cells is to view them as the Creator’s handiwork. For many scientists, it is a road less traveled, but it accounts for all of the data. You can get there from here.

    Resources

    Challenges to the Endosymbiont Hypothesis

    Support for a Creation Model for the Origin of Eukaryotic Cells

    Endnotes
    1. Anja Spang et al., “Complex Archaea that Bridge the Gap between Prokaryotes and Eukaryotes,” Nature 521 (May 14, 2015): 173–79, doi:10.1038/nature14447; Katarzyna Zaremba-Niedzwiedzka et al., “Asgard Archaea Illuminate the Origin of Eukaryotic Cellular Complexity,” Nature 541 (January 19, 2017): 353–58, doi:10.1038/nature21031.
    2. Purificación López-García and David Moreira, “Open Questions on the Origin of Eukaryotes,” Trends in Ecology and Evolution 30, no. 11 (November 2015): 697–708, doi:10.1016/j.tree.2015.09.005.
    3. López-García and Moreira, “Open Questions.”
    4. López-García and Moreira, “Open Questions.”
    5. Laura Villanueva, Stefan Schouten, and Jaap S. Sinninghe Damsté, “Phylogenomic Analysis of Lipid Biosynthetic Genes of Archaea Shed Light on the ‘Lipid Divide,’” Environmental Microbiology 19, no. 1 (January 2017): 54–69, doi:10.1111/1462-2920.13361.
    6. Jonathan Lombard, Purificación López-García, and David Moreira, “The Early Evolution of Lipid Membranes and the Three Domains of Life,” Nature Reviews Microbiology 10 (June 11, 2012): 507–15, doi:10.1038/nrmicro2815.
  • Ancient Mouse Fur Discovery with Mighty Implications

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | Jun 26, 2019

    “What a mouse! . . . WHAT A MOUSE!”

    The narrator’s exclamation became the signature cry each time the superhero Mighty Mouse carried out the most impossible of feats.

    A parody of Superman, Mighty Mouse was the 1942 creation of Paul Terry of Terrytoons Studio for 20th Century Fox. Since then, Mighty Mouse has appeared in theatrical shorts and films, Saturday morning cartoons, and comic books.

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    Figure 1: Mighty Mouse. Image credit: Wikipedia

    Throughout each episode, the characters sing faux arias—mocking opera—with Mighty Mouse belting out, “Here I am to save the day!” each time he flies into action. As you would expect, many of the villains Mighty Mouse battles are cats, with his archnemesis being a feline named Oil Can Harry.

    Mouse Fur Discovery

    Recently, a team of researchers headed by scientists from the University of Manchester in the UK went to heroic measures to detect pigments in a 3-million-year-old mouse fossil, nicknamed—you guessed it—“mighty mouse.”1 To detect the pigments, the researchers developed a new method that employs Synchrotron Rapid Scanning X-Ray Fluorescence Imaging to map metal distributions in the fossil, which, in turn, correlate with the types of pigments found in the animal’s fur when it was alive.

    This work paves the way for paleontologists to develop a better understanding of past life on Earth, with fur pigmentation being unusually important. The color of an animal’s fur has physiological and behavioral importance and can change relatively quickly over the course of geological timescales through microevolutionary mechanisms.

    This discovery also carries importance for the science-faith conversation. Some Christians believe that the recovery of soft tissue remnants, such as the pigments that make up fur, call into question the scientific methods used to determine the age of geological formations and the fossil record. This uncertainty opens up the possibility that our planet (and life on Earth) may be only 6,000 years old.

    Is the young-earth interpretation of this advance valid? Is it possible for soft tissue materials to survive for millions of years? If so, how?

    Detection of 3-Million-Year-Old Pigment

    University of Manchester researchers applied their methodology to an exceptionally well-preserved 3-million-year-old fossil specimen (Apodemus atavus) recovered from the Willershausen conservation site in Germany. The specimen was compressed laterally during the fossilization process and is so well-preserved that imprints of its fur are readily visible.

    The research team indirectly identified the pigments that at one time colored the fur by mapping the distribution of metals in the fossil specimen. These metals are known to associate with the pigments eumelanin and pheomelanin, the two main forms of melanin. (Eumelanin produces black and brown hues. Pheomelanin imparts fur, skin, and feathers with a light reddish-brown color.) As it turns out, copper ions chemically interact with eumelanin and pheomelanin. On the other hand, zinc (Zn) ions interact exclusively with pheomelanin by binding to sulfur (S) atoms that are part of this pigment’s molecular structure. Zinc doesn’t interact with eumelanin because sulfur is not part of its chemical composition.

    The research team mapped the Zn and S distributions of the mighty mouse fossil and concluded that much of the fur was colored with pheomelanin and, therefore, must have been reddish brown. They failed to detect any pigment in the fur coating the animal’s underbelly and feet, leading them to speculate that the mouse had white fur coating its stomach and feet.

    What a piece of science! . . . WHAT A PIECE OF SCIENCE!

    Soft Tissues and the Scientific Case for a Young Earth

    Paleontologists see far-reaching implications for this work. Roy Wogelius, one of the scientists leading the study, hopes that “these results will mean that we can become more confident in reconstructing extinct animals and thereby add another dimension to the study of evolution.”2

    Young-earth creationists (YECs) also see far-reaching implications for this study. Many argue that advances such as this one provide compelling evidence that the earth is young and that the fossil record was laid down as a consequence of a recent global flood.

    The crux of the YEC argument centers around the survivability of soft tissue materials. According to common wisdom, soft tissue materials should rapidly degrade once the organism dies. If this is the case, then there is no way soft tissue remnants should hang around for thousands of years, let alone millions. The fact that these materials can be recovered from fossil specimens indicates that the preserved organisms must be only a few thousand years old. And if thats the case, then the methods used to date the fossils cannot be valid.

    At first glance, the argument carries some weight. Most people find it hard to envision how soft tissue materials could survive for vast periods of time, given the wide range of mechanisms that drive the degradation of biological materials.

    Preservation Mechanisms for Soft Tissues in Fossils

    Despite this initial impression, over the last decade or so paleontologists have identified a number of mechanisms that can delay the degradation of soft tissues long enough for them to become entombed within a mineral shell. When this entombment occurs, the degradation process dramatically slows down. In other words, it is a race against time. Can mineral entombment take place before the soft tissue materials fully decompose? If so, then soft tissue remnants can survive for hundreds of millions of years. And any chemical or physical process that can delay the degradation will contribute to soft tissue survival by giving the entombment process time to take place.

    In Dinosaur Blood and the Age of the Earth, I describe several mechanisms that likely promote soft tissue survival. I also discuss the molecular features that contribute to soft tissue preservation in fossils. Not all molecules are made equally. Some are fragile and some robust. Two molecular properties that make molecules unusually durable are cross-linking and aromaticity. As it turns out, eumelanin and pheomelanin possess both.

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    Figure 2: Chemical Structure of Eumelanin. Image credit: Wikipedia

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    Figure 3: Chemical Structure of Pheomelanin. Image credit: Wikipedia

    When considering the chemical structures of eumelanin and pheomelanin, it isn’t surprising that these materials persist in the fossil record for millions of years. In fact, researchers have isolated eumelanin from a fossilized cephalopod ink sac that dates to around 160 million years ago.3

    It is also worth noting that the mouse specimen was well-preserved, making it even more likely that durable soft-tissue materials would persist in the fossil. And, keep in mind that the research team detected trace amounts of pigments using sophisticated, state-of-the-art chemical instrumentation.

    In short, the recovery of trace levels of soft-tissue materials from fossil remains is not surprising. Soft-tissue materials associated with the mighty mouse specimen—and other fossils, for that matter— can’t save the day for the young-earth paradigm, but they find a ready explanation in an old-earth framework.

    Resources

    Endnotes
    1. Phillip L. Manning et al., “Pheomelanin Pigment Remnants Mapped in Fossils of an Extinct Mammal,” Nature Communications 10, (May 21, 2019): 2250, doi:10.1038/s41467-019-10087-2.
    2. DOE/SLAC National Accelerator Laboratory, “In a First, Researchers Identify Reddish Coloring in an Ancient Fossil,” Science Daily, May 21, 2019, https://www.sciencedaily.com/releases/2019/05/190521075110.htm
    3. Keely Glass et al., “Direct Chemical Evidence for Eumelanin Pigment from the Jurassic Period,” Proceedings of the National Academy of Sciences USA 109, no. 26 (June 26, 2012): 10218–23, doi:10.1073/pnas.1118448109.
  • Satellite DNA: Critical Constituent of Chromosomes

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | Jun 19, 2019

    There is a lot that evolutionary biologists can learn about the purpose of junk DNA from my wife.

    Let me explain.

    Recently, I wound up with a disassembled cabinet in the trunk of my car. Neither my wife Amy nor I could figure out where to put the cabinet in our home and we didn’t want to store it in the garage. The cabinet had all its pieces and was practically new. So, I offered it to a few people, but there were no takers. It seemed that nobody wanted to assemble the cabinet.

    Getting Rid of the Junk

    After driving around with the cabinet pieces in my trunk for a few days, I channeled my inner Marie Kondo. This cabinet wasn’t giving me any joy by taking up valuable space in the trunk. So, I made a quick detour on my way home from the office and donated the cabinet to a charity.

    When I told Amy what I had done, she expressed surprise and a little disappointment. If she had known I was going to donate the cabinet, she would have kept it for its glass doors. In other words, if I hadn’t donated the cabinet, it would have eventually wound up in our garage because it has nice glass doors that Amy thinks she could have repurposed.

    There is a point to this story: The cabinet was designed for a purpose and, at one time, it served a useful function. But once it was disassembled and put in the trunk of my car, nobody seemed to want it. Disassembling the cabinet transformed it into junk. And since my wife loves to repurpose things, she saw a use for it. She didn’t perceive the cabinet as junk at all.

    The moral of my little story also applies to the genomes of eukaryotic organisms. Specifically, is it time that evolutionary scientists view some kinds of DNA not as junk, but rather as purposeful genetic elements?

    Junk in the Genome

    Many biologists hold the view that a vast proportion of the genomes of other eukaryotic organisms is junk, just like the disassembled cabinet I temporarily stored in my car. They believe that, like the unwanted cabinet, many of the different types of “junk” DNA in genomes originated from DNA sequences that at one time performed useful functions. But these functional DNA sequences became transformed (like the disassembled cabinet) into nonfunctional elements.

    Evolutionary biologists consider the existence of “junk” DNA as one of the most potent pieces of evidence for biological evolution. According to this view, junk DNA results when undirected biochemical processes and random chemical and physical events transform a functional DNA segment into a useless molecular artifact. Junk pieces of DNA remain part of an organisms genome, persisting from generation to generation as a vestige of evolutionary history.

    Evolutionary biologists highlight the fact that, in many instances, identical (or nearly identical) segments of junk DNA appear in a wide range of related organisms. Frequently, the identical junk DNA segments reside in corresponding locations in these genomes—and for many biologists, this feature clearly indicates that these organisms shared a common ancestor. Accordingly, the junk DNA segment arose prior to the time that the organisms diverged from their shared evolutionary ancestor and then persisted in the divergent evolutionary lines.

    One challenging question these scientists ask is, Why would a Creator purposely introduce nonfunctional, junk DNA at the exact location in the genomes of different, but seemingly related, organisms?

    Satellite DNA

    Satellite DNA, which consists of nucleotide sequences that repeat over and over again, is one class of junk DNA. This highly repetitive DNA occurs within the centromeres of chromosomes and also in the chromosomal regions adjacent to centromeres (referred to as pericentromeric regions).

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    Figure: Chromosome Structure. Image credit: Shutterstock

    Biologists have long regarded satellite DNA as junk because it doesn’t encode any useful information. Satellite DNA sequences vary extensively from organism to organism. For evolutionary biologists, this variability is a sure sign that these DNA sequences cant be functional. Because if they were, natural selection would have prevented the DNA sequences from changing. On top of that, molecular biologists think that satellite DNAs highly repetitive nature leads to chromosomal instability, which can result in genetic disorders.

    A second challenging question is, Why would a Creator intentionally introduce satellite DNA into the genomes of eukaryotic organisms?

    What Was Thought to Be Junk Turns Out to Have Purpose

    Recently, a team of biologists from the University of Michigan (UM) adopted a different stance regarding the satellite DNA found in pericentromeric regions of chromosomes. In the same way that my wife Amy saw a use for the cabinet doors, the researchers saw potential use for satellite DNA. According to Yukiko Yamashita, the UM research head, “We were not quite convinced by the idea that this is just genomic junk. If we don’t actively need it, and if not having it would give us an advantage, then evolution probably would have gotten rid of it. But that hasn’t happened.”1

    With this mindset—refreshingly atypical for most biologists who view satellite DNA as junk—the UM research team designed a series of experiments to determine the function of pericentromeric satellite DNA.2 Typically, when molecular biologists seek to understand the functional role of a region of DNA, they either alter it or splice it out of the genome. But, because the pericentromeric DNA occupies such a large proportion of chromosomes, neither option was available to the research team. Instead, they made use of a protein found in the fruit fly Drosophila melanogaster, called D1. Previous studies demonstrated that this protein binds to satellite DNA.

    The researchers disabled the gene that encodes D1 and discovered that fruit fly germ cells died. They observed that without the D1 protein, the germ cells formed micronuclei. These structures reflect chromosomal instability and they form when a chromosome or a chromosomal fragment becomes dislodged from the nucleus.

    The team repeated the study, but this time they used a mouse model system. The mouse genome encodes a protein called HMGA1 that is homologous to the D1 protein in fruit flies. When they damaged the gene encoding HMGA1, the mouse cells also died, forming micronuclei.

    As it turns out, both D1 and HMGA1 play a crucial role, ensuring that chromosomes remain bundled in the nucleus. These proteins accomplish this feat by binding to the pericentromeric satellite DNA. Both proteins have multiple binding sites and, therefore, can simultaneously bind to several chromosomes at once. The multiple binding interactions collect chromosomes into a bundle to form an association site called a chromocenter.

    The researchers aren’t quite sure how chromocenter formation prevents micronuclei formation, but they speculate that these structures must somehow stabilize the nucleus and the chromosomes housed in its interior. They believe that this functional role is universal among eukaryotic organisms because they observed the same effects in fruit flies and mice.

    This study teaches us two additional lessons. One, so-called junk DNA may serve a structural role in the cell. Most molecular biologists are quick to overlook this possibility because they are hyper-focused on the informational role (encoding the instructions to make proteins) DNA plays.

    Two, just because regions of the genome readily mutate without consequences doesn’t mean these sequences aren’t serving some kind of functional role. In the case of pericentromeric satellite DNA, the sequences vary from organism to organism. Most molecular biologists assume that because the sequences vary, they must not be functionally important. For if they were, natural selection would have prevented them from changing. But this study demonstrates that DNA sequences can vary—particularly if DNA is playing a structural role—as long as they dont compromise DNA’s structural utility. In the case of pericentromeric DNA, apparently the nucleotide sequence can vary quite a bit without compromising its capacity to bind chromocenter-forming proteins (such as D1 and HMGA1).

    Is the Evolutionary Paradigm the Wrong Framework to Study Genomes?

    Scientists who view biology through the lens of the evolutionary paradigm are often quick to conclude that the genomes of organisms reflect the outworking of evolutionary history. Their perspective causes them to see the features of genomes, such as satellite DNA, as little more than the remnants of an unguided evolutionary process. Within this framework, there is no reason to think that any particular DNA sequence element harbors function. In fact, many life scientists regard these “evolutionary vestiges” as junk DNA. This clearly was the case for satellite DNA.

    Yet, a growing body of data indicates that virtually every category of so-called junk DNA displays function. In fact, based on the available data, a strong case can be made that most sequence elements in genomes possess functional utility. Based on these insights, and the fact that pericentromeric satellite DNA persists in eukaryotic genomes, the team of researchers assumed that it must be functional. Its a clear departure from the way most biologists think about genomes.

    Based on this study (and others like it), I think it is safe to conclude that we really don’t understand the molecular biology of genomes.

    It seems to me that we live in the midst of a revolution in our understanding of genome structure and function. Instead of being a wasteland of evolutionary debris, the architecture and operations of genomes appear to be far more elegant and sophisticated than anyone ever imagined—at least within the confines of the evolutionary paradigm.

    This insight also leads me to wonder if we have been using the wrong paradigm all along to think about genome structure and function. I contend that viewing biological systems as the Creator’s handiwork provides a superior framework for promoting scientific advance, particularly when the rationale for the structure and function of a particular biological system is not apparent. Also, in addressing the two challenging questions, if biological systems have been created, then there must be good reasons why these systems are structured and function the way they do. And this expectation drives further study of seemingly nonfunctional, purposeless systems with the full anticipation that their functional roles will eventually be uncovered.

    Though committed to an evolutionary interpretation of biology, the UM researchers were rewarded with success when they broke ranks with most evolutionary biologists and assumed junk regions of the genome were functional. Their stance illustrates the power of a creation model approach to biology.

    Sadly, most evolutionary biologists are like me when it comes to old furniture. We lack vision and are quick to see it as junk, when in fact a treasure lies in front of us. And, if we let it, this treasure will bring us joy.

    Resources

    Endnotes
    1. University of Michigan, “Scientists Discover a Role for ‘Junk’ DNA,” ScienceDaily (April 11, 2018), www.sciencedaily.com/releases/2018/04/180411131659.htm.
    2. Madhav Jagannathan, Ryan Cummings, and Yukiko M. Yamashita, “A Conserved Function for Pericentromeric Satellite DNA,” eLife 7 (March 26, 2018): e34122, doi:10.7554/eLife.34122.
  • Frog Choruses Sing Out a Song of Creation

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | Jun 12, 2019

    My last name, Rana, is Sanskrit in origin, referring to someone who descends from the Thar Ghar aristocracy. Living in Southern California means I don’t often meet Urdu-speaking people who would appreciate the regal heritage connected to my family name. But I do meet a lot of Spanish speakers. And when I introduce myself, I often see raised eyebrows and smiles.

    In Spanish, Rana means frog.

    My family has learned to embrace our family’s namesake. In fact, when our kids were little, my wife affectionately referred to our five children as ranitas—little frogs.

     

     

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    Image: Five Ranitas. Image credit: Shutterstock

    Our feelings about these cute and colorful amphibians aside, frogs are remarkable creatures. They engage in some fascinating behaviors. Take courtship, as an example. In many frog species, the males croak to attract the attention of females, with each frog species displaying its own distinct call.

    Male frogs croak by filling their vocal sacs with air. This allows them to amplify their croaks for up to a mile away. Oftentimes, male frogs in the same vicinity will all croak together, forming a chorus.

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    Image: Male Frog Croaking to Attract a Female. Image credit: Shutterstock

    As it turns out, female frogs aren’t the only ones who respond to frog croaks.

    A research team from Japan has spent a lot of time listening to and analyzing frog choruses with the hopes of understanding the mathematical structure of the sounds that frogs collectively make when they call out to females. Once they had the mathematical model in hand, the researchers discovered that they could use it to improve the efficiency of wireless data transfer systems.1

    This work serves as one more example of scientists and engineers applying insights from biology to drive technology advances and breakthroughs. This approach to technology development (called biomimetics and bioinspiration)—exemplified by the impressive work of the Japanese researchers—has significance that extends beyond engineering. It can be used to make the case that a Creator must have played a role in the design and history of life by marshaling support for two distinct arguments for God’s existence:

    Frog Choruses: A Cacophony or a Symphony?

    Anyone who has spent time near a pond at night certainly knows the ruckus that an army of male frogs can make when each of them is vying for the attention of females.

    All the male frogs living near the pond want to attract females to the same breeding site, but, in doing so, each individual also wants to attract females to his specific territory. Field observations indicate that, instead of engaging in a croaking free-for-all (with neighboring frogs trying to outperform one another), the army of frogs engages in a carefully orchestrated acoustical presentation. As a result, male frogs avoid call overlap with neighboring males on a short timescale, while synchronizing their croaks with the other frogs to produce a chorus on a longer timescale.

    The frogs avoid call overlap by alternating between silence and croaking, coordinating with neighboring frogs so that when one frog rests, another croaks. This alternating back-and-forth makes it possible for each individual frog to be heard amid the chorus, and it also results in a symphonic chorus of frog croaks.

    The Mathematical Structure of Frog Choruses

    To dissect the mathematical structure of frog choruses, the research team placed three male Japanese tree frogs into individual mesh cages that were set along a straight line, with a two-foot separation between each cage. The researchers recorded the frog’s croaks using microphones placed by each cage.

    They observed that all three frogs alternated their calls, forming a triphasic synchronization. One frog croaked continuously for a brief period of time and then would rest, while the other two frogs took their turn croaking and resting. The researchers determined that the rest breaks for the frogs were important because of the amount of energy it takes the frogs to produce a call.

    All three frogs would synchronize the start and stop of their calls to produce a chorus followed by a period of silence. They discovered that the time between choruses varied quite a bit, without rhyme or reason, and was typically much longer than the chorus time. On the other hand, the croaking of each individual lasted for a predictable time duration that was followed immediately by the croaking of a neighboring frog.

    By analyzing the acoustical data, the researchers developed a mathematical model to describe the croaking of individual frogs and the collective behavior of the frogs when they belted out a chorus of calls. Their model consisted of both deterministic and stochastic components.

    Use of Frog Choruses for Managing Data Traffic

    The researchers realized that the mathematical model they developed could be applied to control wireless sensor networks, such as those that make up the internet of things. These networks entail an array of sensor nodes that transmit data packets, delivering them to a gateway node by multi-hop communication, with data packets transmitted from sensor to sensor until it reaches the gate. During transmission, it is critical for the system to avoid the collision of data packets. It is also critical to regulate the overall energy consumption of the system, to avoid wasting valuable energy resources.

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    Image: The Internet of Things Made Up of Wireless Sensors. Image credit: Shutterstock

    Through simulation studies, the Japanese team demonstrated that the mathematical model inspired by frog choruses averted the collision of data packets in a wireless sensor array, maximized network connectivity, and enhanced efficiency of the array by minimizing power consumption. The researchers conclude, “This study highlights the unique dynamics of frog choruses over multiple time scales and also provides a novel bio-inspired technology.”2

    As important as this work may be for inspiring new technologies, as a Christian, I find its real significance in the theological arena.

    Frog Choruses and the Argument from Beauty

    The grandeur of nature touches the very core of who we are—if we take the time to let it. But, as the work by the Japanese researchers demonstrates, the grandeur we see all around us in nature isn’t confined to what we perceive with our immediate senses. It exists in the underlying mathematical structure of nature. It is nothing short of amazing to think that such exquisite organization and orchestration characterizes frog choruses, so much so that it can inspire sophisticated data management techniques.

    From my vantage point, the beauty and mathematical elegance of nature points to the reality of a Creator.

    If God created the universe, then it is reasonable to expect it to be a beautiful universe, one that displays an even deeper underlying beauty in the mathematical structure that defines the universe itself and phenomena within the universe. Yet if the universe came into existence through mechanism alone, there isn’t any real reason to think it would display beauty. In other words, the beauty in the world around us signifies the divine.

    Furthermore, if the universe originated through uncaused physical mechanisms, there is no reason to think that humans would possess an appreciation for beauty.

    A quick survey of the scientific and popular literature highlights the challenge that the origin of our aesthetic sense creates for the evolutionary paradigm.3 Plainly put: evolutionary biologists have no real explanation for the origin of our aesthetic sense. To be clear, evolutionary biologists have posited explanations to account for the genesis of our capacity to appreciate beauty. But after examining these ideas, we walk away with the strong sense that they are not much more than “just-so stories,” lacking any real evidential support.

    On the other hand, if human beings are made in God’s image, as Scripture teaches, we should be able to discern and appreciate the universe’s beauty, made by our Creator to reveal his glory and majesty.

    Frog Choruses and the Converse Watchmaker Argument

    The idea that biological designs—such as the courting behavior of male frogs—can inspire engineering and technology advances is also highly provocative for other reasons. First, it highlights just how remarkable and elegant the designs found throughout the living realm actually are.

    I think that the elegance of these designs points to a Creator’s handiwork. It also makes possible a new argument for God’s existence—one I have named the converse Watchmaker argument. (For a detailed discussion, see my essay titled “The Inspirational Design of DNA” in the book Building Bridges.)

    The argument can be stated like this:

    • If biological designs are the work of a Creator, then these systems should be so well-designed that they can serve as engineering models for inspiring the development of new technologies.
    • Indeed, this scenario plays out in the engineering discipline of biomimetics.
    • Therefore, it becomes reasonable to think that biological designs are the work of a Creator.

    In fact, I will go one step further. Biomimetics and bioinspiration logically arise out of a creation model approach to biology. That designs in nature can be used to inspire engineering makes sense only if these designs arose from an intelligent Mind. The mathematical structure of frog choruses is yet another example of such bioinspiration.

    Frogs really are amazing—and regal—creatures. Listening to a frog chorus can connect us to the beauty of the world around us. And it will one day help all of our electronic devices to connect together. And that’s certainly something to sing about.

    Resources

    Endnotes
    1. Ikkyu Aihara et al., “Mathematical Modelling and Application of Frog Choruses As an Autonomous Distributed Communication System, Royal Society Open Science 6, no. 1 (January 2, 2019): 181117, doi:10.1098/rsos.181117.
    2. Aihara et al., “Mathematical Modelling and Application.
    3. For example, see Ferris Jabr, “How Beauty is Making Scientists Rethink Evolution,” The New York Times Magazine, January 9, 2019, https://www.nytimes.com/2019/01/09/magazine/beauty-evolution-animal.html.
  • Why Would God Create a World with Parasites?

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | Jun 05, 2019

    A being so powerful and so full of knowledge as a God who could create the universe, is to our finite minds omnipotent and omniscient, and it revolts our understanding to suppose that his benevolence is not unbounded, for what advantage can there be in the sufferings of millions of lower animals throughout almost endless time? This very old argument from the existence of suffering against the existence of an intelligent first cause seems to me a strong one; whereas, as just remarked, the presence of much suffering agrees well with the view that all organic beings have been developed through variation and natural selection.1

    —Charles Darwin, The Autobiography of Charles Darwin

    If God exists and if he is all-powerful, all-knowing, and all-good, why is there so much pain and suffering in the world? This conundrum keeps many skeptics and seekers from the Christian faith and even troubles some Christians.

    Perhaps nothing epitomizes the problem of pain and suffering more than the cruelty observed in nature. Indeed, what advantage can there be in the suffering of millions of animals?

    Often, the pain and suffering animals experience is accompanied by unimaginable and seemingly unnecessary cruelty.

    Take nematodes (roundworms) as an example. There are over 10,000 species of nematodes. Some are free-living. Others are parasitic. Nematode parasites infect humans, animals, plants, and insects, causing untold pain and suffering. But their typical life cycle in insects seems especially cruel.

    Nematodes that parasitize insects usually are free-living in their adult form but infest their host in the juvenile stage. The infection begins when the juvenile form of the parasite enters into the insect host, usually through a body opening, such as the mouth or anus. Sometimes the juveniles drill through the insect’s cuticle.

    Once inside the host, the juveniles release bacteria that infect and kill the host, liquefying its internal tissues. As long as the supply of host tissue holds out, the juveniles will live within the insect’s body, even reproducing. When the food supply runs out, the nematodes exit the insect and seek out another host.

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    Figure 1: An Entomopathogenic Nematode Juvenile. Image credit: Shutterstock

    Why would God create a world with parasitism? Could God really be responsible for a world like the one we inhabit? Many skeptics would answer “no” and conclude that God must not exist.

    A Christian Response to the Problem of Evil

    One way to defend God’s existence and goodness in the face of animal pain and suffering is to posit that there just might be good reasons for God to create the world the way it is. Perhaps what we are quick to label as evil may actually serve a necessary function.

    This perspective gains support based on some recent insights into the benefits that insect parasites impart to ecosystems. A research team from the University of Georgia (UGA) recently unearthed one example of the important role played by these parasites.2 These researchers demonstrated that nematode-infected horned passalus beetles (bess beetles) are more effective at breaking down dead logs in the forest than their parasite-free counterparts—and this difference benefits the ecosystem. Here’s how.

    The Benefit Parasites Provide to the Ecosystem

    The horned passalus lives in decaying logs. The beetles consume wood through a multistep process. After ingesting the wood, these insects excrete it in a partially digested form. The wood excrement becomes colonized by bacteria and fungi and then is later re-consumed by the beetle.

    These insects can become infected by a nematode parasite (Chondronema passali). The parasite inhabits the abdominal cavity of the beetle (though not its gastrointestinal tract). When infected, the horned passalus can harbor thousands of individual nematodes.

    To study the effect of this parasite on the horned passalus and the forest ecosystem inhabited by the insect, researchers collected 113 individuals from the woods near the UGA campus. They also collected pieces of wood from the logs bearing the beetles.

    In the laboratory, they placed each of the beetles in separate containers that also contained pieces of wood. After three months, they discovered that the beetles infected with the nematode parasite processed 15 percent more wood than beetles that were parasite-free. Apparently, the beetles compensate for the nematode infection by consuming more food. One possible reason for the increased wood consumption may be due to the fact that the parasites draw away essential nutrients from the beetle host, requiring the insect to consume more food.

    While it isn’t clear if the parasite infestation harms the beetle (infected beetles have reduced mobility and loss of motor function), it is clear that the infestation benefits the ecosystem. These beetles play a key role in breaking down dead logs and returning nutrients to the forest soil. By increasing the beetles wood consumption, the nematodes accelerate this process, benefiting the ecosystem’s overall health.

    Cody Prouty, one of the projects researchers, points out “that although the beetle and the nematode have a parasitic relationship, the ecosystem benefits from not only the beetle performing its function, but the parasite increasing the efficiency of the beetle. Over the course of a few years, the parasitized beetles could process many more logs than unparasitized beetles, and lead to an increase of organic matter in soils.”3

    This study is not the first to discover benefits parasites impart to ecosystems. Parasites play a role in shaping ecosystem biodiversity and they intertwine with the food web. The researchers close their article this way: “Countering long-standing unpopular views of parasites is certainly challenging, but perhaps evidence like that presented here will be of use in this effort.”4

    Such evidence does not revolt our understanding, as Darwin might suggest, but instead enhances our insights into the creation and helps counter the challenge of the problem of evil. Even creatures as gruesome as parasites can serve a beneficial purpose in creation and maybe could rightfully be understood as good.

    Resources

    Endnotes
    1. Charles Darwin, The Autobiography of Charles Darwin: 1809–1882 (New York: W. W. Norton, 1969), 90.
    2. Andrew K. Davis and Cody Prouty, “The Sicker the Better: Nematode-Infected Passalus Beetles Provide Enhanced Ecosystem Services, Biology Letters 15, no. 5 (2019): 20180842, doi:10.1098/rsbl.2018.0842.
    3. University of Georgia, “Parasites Help Beetle Hosts Function More Effectively,” ScienceDaily (May 1, 2019), https://www.sciencedaily.com/releases/2019/05/190501131435.htm.
    4. Davis and Prouty,“The Sicker the Better,” 3.
  • Biochemical Grammar Communicates the Case for Creation

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | May 29, 2019

    As I get older, I find myself forgetting things—a lot. But, thanks to smartphone technology, I have learned how to manage my forgetfulness by using the “Notes” app on my iPhone.

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    Figure 1: The Apple Notes app icon. Image credit: Wikipedia

    This app makes it easy for me to:

    • Jot down ideas that suddenly come to me
    • List books I want to read and websites I want to visit
    • Make note of musical artists I want to check out
    • Record “to do” and grocery lists
    • Write down details I need to have at my fingertips when I travel
    • List new scientific discoveries with implications for the RTB creation model that I want to blog about, such as the recent discovery of a protein grammar calling attention to the elegant design of biochemical systems

    And the list goes on. I will never forget, again!

    On top of that, I can use the Notes app to categorize and organize all my notes and house them in a single location. Thus, I don’t have to manage scraps of paper that invariably wind up getting scattered all over the place—and often lost.

    And, as a bonus, the Notes app anticipates the next word I am going to use even before I type it. I find myself relying on this feature more and more. It is much easier to select a word than type it out. In fact, the more I use this feature, the better the app becomes at anticipating the next word I want to type.

    Recently, a team of bioinformaticists from the University of Alabama, Birmingham (UAB) and the National Institutes of Health (NIH) used the same algorithm the Notes app uses to anticipate word usage to study protein architectures.1 Their analysis reveals new insight into the structural features of proteins and also highlights the analogy between the information housed in these biomolecules and human language. This analogy contributes to the revitalized Watchmaker argument presented in my book The Cell’s Design.

    N-Gram Language Modeling

    The algorithm used by the Notes app to anticipate the next word the user will likely type is called n-gram language modeling. This algorithm determines the probability of a word being used based on the previous word (or words) typed. (If the probability is based on a single word, it is called a unigram probability. If the calculation is based on the previous two words, it is called a bigram probability, and so on.) This algorithm “trains” the Notes app so that the more I use it, the more reliable the calculated probabilities—and, hence, the better the word recommendations.

    N-Gram Language Modeling and the Case for a Creator

    To understand why the work of research team from UAB and NIH provides evidence for a Creator’s role in the origin and design of life, a brief review of protein structure is in order.

    Protein Structure

    Proteins are large complex molecules that play a key role in virtually all of the cell’s operations. Biochemists have long known that the three-dimensional structure of a protein dictates its function.

    Because proteins are such large complex molecules, biochemists categorize protein structure into four different levels: primary, secondary, tertiary, and quaternary structures. A protein’s primary structure is the linear sequence of amino acids that make up each of its polypeptide chains.

    The secondary structure refers to short-range three-dimensional arrangements of the polypeptide chain’s backbone arising from the interactions between chemical groups that make up its backbone. Three of the most common secondary structures are the random coil, alpha (α) helix, and beta (β) pleated sheet.

    Tertiary structure describes the overall shape of the entire polypeptide chain and the location of each of its atoms in three-dimensional space. The structure and spatial orientation of the chemical groups that extend from the protein backbone are also part of the tertiary structure.

    Quaternary structure arises when several individual polypeptide chains interact to form a functional protein complex.

     

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    Figure 2: The four levels of protein structure. Image credit: Shutterstock

    Protein Domains

    Within the tertiary structure of proteins, biochemists have discovered compact, self-contained regions that fold independently. These three-dimensional regions of the protein’s structure are called domains. Some proteins consist of a single compact domain, but many proteins possess several domains. In effect, domains can be thought to be the fundamental units of a protein’s tertiary structure. Each domain possesses a unique biochemical function. Biochemists refer to the spatial arrangement of domains as a protein’s domain architecture.

    Researchers have discovered several thousand distinct protein domains. Many of these domains recur in different proteins, with each protein’s tertiary structure comprised of a mix-and-match combination of protein domains. Biochemists have also learned that a relationship exists between the complexity of an organism and the number of unique domains found in its set of proteins and the number of multi-domain proteins encoded by its genome.

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    Figure 3: Pyruvate kinase, an example of a protein with three domains. Image credit: Wikipedia

    The Key Question in Protein Chemistry

    As much progress as biochemists have made characterizing protein structure over the last several decades, they still lack a fundamental understanding of the relationship between primary structure (the amino acid sequence) and tertiary structure and, hence, protein function. In order to develop this insight, they need to determine the “rules” that dictate the way proteins fold. Treating proteins as information systems can help determine some of these rules.

    Protein as Information Systems

    Proteins are not only large, complex molecules but also information-harboring systems. The amino acid sequence that defines a protein’s primary structure is a type of information—biochemical information—with the individual amino acids analogous to the letters that make up an alphabet.

    N-Gram Analysis of Proteins

    To gain insight into the relationship between a protein’s primary structure and its tertiary structures, the researchers from UAB and NIH carried out an n-gram analysis on the 23 million protein domains found in the protein sets of 4,800 species found across all three domains of life.

    These researchers point out that an individual amino acid in a protein’s primary structure doesn’t contain information just as an individual letter in an alphabet doesn’t harbor any meaning. In human language, the most basic unit that conveys meaning is a word. And, in proteins, the most basic unit that conveys biochemical meaning is a domain.

    To decipher the “grammar” used by proteins, the researchers treated adjacent pairs of protein domains in the tertiary structure of each protein in the sample set as a bigram (similar to two words together). Surveying the proteins found in their data set of 4,800 species, they discovered that 95% of all the possible domain combinations don’t exist!

    This finding is key. It indicates that there are, indeed, rules that dictate the way domains interact. In other words, just like certain word combinations never occur in human languages because of the rules of grammar, there appears to be a protein “grammar” that constrains the domain combinations in proteins. This insight implies that physicochemical constraints (which define protein grammar) dictate a protein’s tertiary structure, preventing 95% of conceivable domain-domain interactions.

    Entropy of Protein Grammar

    In thermodynamics, entropy is often used as a measure of the disorder of a system. Information theorists borrow the concept of entropy and use it to measure the information content of a system. For information theorists, the entropy of a system is indirectly proportional to the amount of information contained in a sequence of symbols. As the information content increases, the entropy of the sequence decreases, and vice versa. Using this concept, the UAB and NIH researchers calculated the entropy of the protein domain combinations.

    In human language, the entropy increases as the vocabulary increases. This makes sense because, as the number of words increases in a language, the likelihood that random word combinations would harbor meaning decreases. In like manner, the research team discovered that the entropy of the protein grammar increases as the number of domains increases. (This increase in entropy likely reflects the physicochemical constraints—the protein grammar, if you will—on domain interactions.)

    Human languages all carry the same amount of information. That is to say, they all display the same entropy content. Information theorists interpret this observation as an indication that a universal grammar undergirds all human languages. It is intriguing that the researchers discovered that the protein “languages” across prokaryotes and eukaryotes all display the same level of entropy and, consequently, the same information content. This relationship holds despite the diversity and differences in complexity of the organism in their data set. By analogy, this finding indicates that a universal grammar exists for proteins. Or to put it another way, the same set of physicochemical constraints dictate the way protein domains interact for all organisms.

    At this point, the researchers don’t know what the grammatical rules are for proteins, but knowing that they exist paves the way for future studies. It also generates hope that one day biochemists might understand them and, in turn, use them to predict protein structure from amino acid sequences.

    This study also illustrates how fruitful it can be to treat biochemical systems as information systems. The researchers conclude that “The similarities between natural languages and genomes are apparent when domains are treated as functional analogs of words in natural languages.”2

    In my view, it is this relationship that points to a Creator’s role in the origin and design of life.

    Protein Grammar and the Case for a Creator

    As discussed in The Cell’s Design, the recognition that biochemical systems are information-based systems has interesting philosophical ramifications. Common, everyday experience teaches that information derives solely from the activity of human beings. So, by analogy, biochemical information systems, too, should come from a divine Mind. Or at least it is rational to hold that view.

    But the case for a Creator strengthens when we recognize that it’s not merely the presence of information in biomolecules that contributes to this version of a revitalized Watchmaker analogy. Added vigor comes from the UAB and NIH researchers’ discovery that the mathematical structure of human languages and biochemical languages is identical.

    Skeptics often dismiss the updated Watchmaker argument by arguing that biochemical information is not genuine information. Instead, they maintain that when scientists refer to biomolecules as harboring information, they are employing an illustrative analogy—a scientific metaphor—and nothing more. They accuse creationists and intelligent design proponents of misconstruing their use of analogical language to make the case for design.3

    But the UAB and NIH scientists’ work questions the validity of this objection. Biochemical information has all of the properties of human language. It really is information, just like the information we conceive and use to communicate.

    Is There a Biochemical Anthropic Principle?

    This discovery also yields another interesting philosophical implication. It lends support to the existence of a biochemical anthropic principle. Discovery of a protein grammar means that there are physicochemical constraints on protein structure. It is remarkable to think that protein tertiary structures may be fundamentally dictated by the laws of nature, instead of being the outworking of an historically contingent evolutionary history. To put it differently, the discovery of a protein grammar reveals that the structure of biological systems may reflect some deep, underlying principles that arise from the very nature of the universe itself. And yet these structures are precisely the types of structures life needs to exist.

    I interpret this “coincidence” as evidence that our universe has been designed for a purpose. And as a Christian, I find that notion to resonate powerfully with the idea that life manifests from an intelligent Agent—namely, God.

    Resources to Dig Deeper

    Endnotes
    1. Lijia Yu et al., “Grammar of Protein Domain Architectures,” Proceedings of the National Academy of Sciences, USA 116, no. 9 (February 26, 2019): 3636–45, doi:10.1073/pnas.1814684116.
    2. Yu et al., 3636–45.
    3. For example, see Massimo Pigliucci and Maarten Boudry, “Why Machine-Information Metaphors Are Bad for Science and Science Education,” Science and Education 20, no. 5–6 (May 2011): 453–71; doi:10.1007/s11191-010-9267-6.
  • Why Would God Create a World Where Animals Eat Their Offspring?

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | May 22, 2019

    What a book a Devil’s chaplain might write on the clumsy, wasteful, blundering, low and horridly cruel works of nature!

    –Charles Darwin, “Letter to J. D. Hooker,” Darwin Correspondence Project

    You may not have ever heard of him, but he played an important role in ushering in the Darwinian revolution in biology. His name was Asa Gray.

    Gray (1810–1888) was a botanist at Harvard University. He was among the first scientists in the US to adopt Darwin’s theory of evolution. Asa Gray was also a devout Christian.

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    Asa Gray in 1864. Image credit: John Adams Whipple, Wikipedia

    Gray was convinced that Darwin’s theory of evolution was sound. He was also convinced that nature displayed unmistakable evidence for design. For this reason, he reasoned that God must have used evolution as the means to create and, in doing so, Gray may have been the first person to espouse theistic evolution.

    In his book Darwinia, Asa Gray presents a number of essays defending Darwin’s theory. Yet, he also expresses his deepest convictions that nature is filled with indicators of design. He attributed that design to a type of God-ordained, God-guided process. Gray argued that God is the source of all evolutionary change.

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    Gray and Darwin struck up a friendship and exchanged around 300 letters. In the midst of their correspondence, Gray asked Darwin if he thought it possible that God used evolution as the means to create. Darwins reply revealed that he wasn’t very impressed with this idea.

    I cannot persuade myself that a beneficent & omnipotent God would have designedly created the Ichneumonidæ with the express intention of their feeding within the living bodies of caterpillars, or that a cat should play with mice. Not believing this, I see no necessity in the belief that the eye was expressly designed. On the other hand I cannot anyhow be contented to view this wonderful universe & especially the nature of man, & to conclude that everything is the result of brute force. I am inclined to look at everything as resulting from designed laws, with the details, whether good or bad, left to the working out of what we may call chance. Not that this notion at all satisfies me. I feel most deeply that the whole subject is too profound for the human intellect. A dog might as well speculate on the mind of Newton. Let each man hope & believe what he can.1

    Darwin could not embrace Gray’s theistic evolution because of the cruelty he saw in nature that seemingly causes untold pain and suffering in animals. Darwin—along with many skeptics today—couldn’t square a world characterized by that much suffering with the existence of a God who is all-powerful, all-knowing, and all-good.

    Filial Cannibalism

    The widespread occurrence of filial cannibalism (when animals eat their young or consume their eggs after laying them) and abandonment (leading to death) exemplify such cruelty in animals. It seems such a low and brutal feature of nature.

    Why would God create animals that eat their offspring and abandon their young?

    Is Cruelty in Nature Really Evil?

    But what if there are good reasons for God to allow pain and suffering in the animal kingdom? I have written about good scientific reasons to think that a purpose exists for animal pain and suffering (see “Scientists Uncover a Good Purpose for Long-Lasting Pain in Animals” by Fazale Rana).

    And, what if animal death is a necessary feature of nature? Other studies indicate that animal death promotes biodiversity and ecosystem stability (see “Of Weevils and Wasps: God’s Good Purpose in Animal Death” by Maureen Moser, and “Animal Death Prevents Ecological Meltdown” by Fazale Rana).

    There also appears to be a reason for filial cannibalism and offspring abandonment, at least based on a study by researchers from Oxford University (UK) and the University of Tennessee.2 These researchers demonstrated that filial cannibalism and offspring abandonment comprise a form of parental care.

    What? How is that conclusion possible?

    It turns out that when animals eat their offspring or abandon their young, the reduction promotes the survival of the remaining offspring. To arrive at this conclusion, the researchers performed mathematical modeling of a generic egg-laying species. They discovered that when animals sacrificed a few of their young, the culling led to greater fitness for their offspring than when animals did not engage in filial cannibalism or egg abandonment.

    These behaviors become important when animals lay too many eggs. In order to properly care for their eggs (protect, incubate, feed, and clean), animals confine egg-laying to a relatively small space. This practice leads to a high density of eggs. But this high density can have drawbacks, making the offspring more vulnerable to diseases and lack of sufficient food and oxygen. Filial cannibalism reduces the density, ensuring a greater chance of survival for those eggs that are left behind. So, ironically, when egg density is too high for the environmental conditions, more offspring survive when the parents consume some, rather than none, of the eggs.

    So, why lay so many eggs in the first place?

    In general, the more eggs that are laid, the greater the number of surviving offspring—assuming there are unlimited resources and no threats of disease. But it is difficult for animals to know how many eggs to lay because the environment is unpredictable and constantly changing. A better way to ensure reproductive fitness is to lay more eggs and remove some of them if the environment can’t sustain the egg density.

    So, it appears as if there is a good reason for God to create animals that eat their young. In fact, you might even argue that filial cannibalism leads to a world with less cruelty and suffering than a world where filial cannibalism doesnt exist at all. This feature of nature is consistent with the idea of an all-powerful, all-knowing, and all-good God who has designed the creation for his good purposes.

    Resources

    Endnotes
    1. To Asa Gray 22 May [1860],” Darwin Correspondence Project, University of Cambridge, accessed May 15, 2019, https://www.darwinproject.ac.uk/letter/DCP-LETT-2814.xml.
    2. Mackenzie E. Davenport, Michael B. Bansall, and Hope Klug, “Unconventional Care: Offspring Abandonment and Filial Cannibalism Can Function as Forms of Parental Care,Frontiers in Ecology and Evolution 7 (April 17, 2019): 113, doi:10.3389/fevo.2019.00113.
  • Competitive Endogenous RNA Hypothesis Supports the Case for Creation

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | May 15, 2019

    When Francis Crick, codiscoverer of the DNA double helix, first conceived of molecular biology’s organizing principle in 1958, he dubbed it the central dogma. He soon came to regret the term. In his autobiographical account, What Mad Pursuit, Crick writes:

    I called this idea the central dogma, for two reasons, I suspect. I had already used the obvious word hypothesis in the sequence hypothesis, and in addition I wanted to suggest that this new assumption was more central and more powerful….As it turned out, the use of the word dogma caused almost more trouble than it was worth. Many years later Jacques Monod pointed out to me that I did not appear to understand the correct use of the word dogma, which is a belief that cannot be doubted. I did apprehend this in a vague sort of way but since I thought that all religious beliefs were without foundation, I used the word the way I myself thought about it, not as most of the world does, and simply applied it to a grand hypothesis that, however plausible, had little direct experimental support.1

    Even though Crick rued labeling his idea as “dogma,” the term seems to fit, all the connotations aside, because of its singular importance to molecular biology.

    The Central Dogma of Molecular Biology

    The central dogma of molecular biology describes the directional flow of information in the cell, which moves from DNA to RNA to proteins. Information can flow from DNA to DNA during DNA replication, from DNA to RNA during transcription, and from RNA back to DNA during reverse transcription. However, biochemical information can’t flow from proteins to either RNA or DNA.

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    Figure 1: The Central Dogma of Molecular Biology. Image credit: Shutterstock

    Is There a New Dogma in Molecular Biology?

    In my opinion as a biochemist, if there is an idea that has the potential to rival the significance of the central dogma, it just might be the competitive endogenous RNA (ceRNA) hypothesis. This newer model provides a comprehensive description of the role messenger RNA (mRNA) molecules play in regulating gene expression, thereby influencing the flow of information from DNA to proteins.

    The ceRNA hypothesis also provides an elegant rationale for why the genomes of eukaryotic organisms contain pseudogenes (including unitary pseudogenes) and encode long noncoding RNA molecules. Additionally, it explains why duplicated pseudogenes resemble corresponding intact genes. In doing all this, the ceRNA hypothesis provides support for the RTB’s genomics model—which interprets the structure and activities associated with genomes from a creation or design standpoint. (An overview of the RTB genomics model can be found in the updated and expanded 2nd edition of Who Was Adam?)

    The Competitive Endogenous RNA Hypothesis

    I discuss the ceRNA hypothesis in a previous article. So, I’ll offer just a brief description here. According to the central dogma, the final step in the flow of biochemical information is the production of proteins at the ribosome, directed by the information housed in mRNA. Biochemists have discovered an elaborate mechanism that selectively degrades mRNA transcripts before they can reach this point. This degradation process controls gene expression by dictating the amount of protein produced.

    Molecules called microRNAs bind to the mRNA’s 3′ untranslated region, which flags the transcript for destruction by RNA-induced silencing complex (RISC). A number of distinct microRNA species exist in the cell. Each microRNA species bind to specific sites in the 3′ untranslated region of mRNA transcripts. (These binding locations are called microRNA response elements or MREs.)

    A network of genes shares the same set of MREs and, consequently, will bind to the same set of microRNAs. When one gene is transcribed, it will influence the expression of all the other genes in its network. And when one gene in the network becomes up-regulated (leading to increased transcription of that gene), the expression of all the genes in the network increases. Why? Because the increased level of that particular transcript exerts a “sponge effect” that consumes more of the microRNAs that would otherwise target other transcripts for degradation.

    The Competitive Endogenous RNA Hypothesis and the Role of Junk DNA

    The ceRNA hypothesis elegantly explains the functional utility of three classes of junk DNA: duplicated and unitary pseudogenes, plus long noncoding RNAs. As it turns out, the transcripts produced from these types of so-called junk DNA also harbor MREs. None of these transcripts codes for proteins yet they play an indispensable role in regulating gene expression. In fact, all three are much better suited for the role of molecular sponges precisely because they aren’t translated into proteins.

    Of particular utility are duplicated pseudogenes due to their close structural resemblance to the corresponding coding genes. Duplicated pseudogenes not only exert a sponge effect but also serve as decoys that allow the transcripts of the intact genes to escape degradation and to be translated into proteins.

    Is the Competitive Endogenous RNA Hypothesis Valid?

    This question has generated a minor scientific controversy. Some studies provide experimental support for this idea while others question the physiological relevance of ceRNAs. In light of this debate, a team of researchers headed by investigators from Columbia University sought to validate this hypothesis on a large-scale.2 They discovered that ceRNA interactions can disrupt the expression of thousands of genes. The team concluded that “ceRNA regulation is the norm not the exception…and that ceRNA interactions have genome-wide effects on gene expression.”3

    These researchers think that this insight sheds light on tumor biology because dysregulation of ceRNAs have been implicated in some cancers. Their work also has theological significance because it undermines one of the most significant challenges to design arguments and, in turn, can be marshaled in support of the RTB genomics model.

    The Competitive Endogenous Hypothesis and the Case for a Creator

    Evolutionary biologists have long maintained that identical (or nearly identical) junk DNA sequences (such as pseudogene sequences) found in corresponding locations in genomes of organisms that naturally cluster together (such as humans and the great apes) provide compelling evidence that these organisms must have evolved from a shared ancestor. This interpretation was compelling because junk DNA sequences seemed to be useless vestiges of evolutionary history.

    Creationists and intelligent design proponents had little to offer by way of evidence for the intentional design of genomes. But research in recent years has revealed that virtually every class of junk DNA has function. It seems, then, that shared junk DNA sequences can be understood as shared designs, which is what the RTB genomics model predicts.

    Additionally, the ceRNA hypothesis supports the RTB genomics even further. This hypothesis provides an elegant explanation for the widespread existence of pseudogenes in genomes and their structural similarity to intact genes.

    Could it be that the idea of religious dogma affirming a Creator’s role in life’s design and history has merit?

    Resources

    Endnotes
    1. Francis Crick, What Mad Pursuit (New York: Basic Books, 1988), 109.
    2. Hua-Sheng Chiu et al., “High-Throughput Validation of ceRNA Regulatory Networks,” BMC Genomics 18 (2017): 418, doi:10.1186/s12864-017-3790-7.
    3. Chiu et al., 418.
  • Pseudogene Discovery Pains Evolutionary Paradigm

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | May 08, 2019

    It was one of the most painful experiences I ever had. A few years ago, I had two back-to-back bouts of kidney stones. I remember it as if it were yesterday. Man, did it hurt when I passed the stones! All I wanted was for the emergency room nurse to keep the Demerol coming.

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    Figure 1: Schematic Depiction of Kidney Stones Moving through the Urinary Tract. Image Credit: Shutterstock

    When all that misery was going down, I wished I was one of those rare individuals who doesn’t experience pain. There are some people who, due to genetic mutations, live pain-free lives. This condition is called hypoalgesia. (Of course, there is a serious downside to hypoalgesia. Pain lets us know when our body is hurt or sick. Because hypoalgesics can’t experience pain, they are prone to serious injury, etc.)

    Biomedical researchers possess a keen interest in studying people with hypoalgesia. Identifying the mutations responsible for this genetic condition helps investigators understand the physiological processes that undergird the pain sensation. This insight then becomes indispensable to guiding efforts to develop new drugs and techniques to treat pain.

    By studying the genetic profile of a 66-year-old woman who lived a lifetime with pain-free injuries, a research team from the UK recently discovered a novel genetic mutation that causes hypoalgesia.1 The mutation responsible for this patient’s hypoalgesia occurred in a pseudogene, a region of the genome considered nonfunctional “junk DNA.”

    This discovery adds to the mounting evidence that shows junk DNA is functional. At this point, molecular geneticists have demonstrated that virtually every class of junk DNA has function. This notion undermines the best evidence for common descent and, hence, undermines an evolutionary interpretation of biology. More importantly, the discovery adds support for the competitive endogenous RNA hypothesis, which can be marshaled to support RTB’s genomics model. It is becoming more and more evident to me that genome structure and function reflect the handiwork of a Creator.

    The Role of a Pseudogene in Mediating Hypoalgesia

    To identify the genetic mutation responsible for the 66-year-old’s hypoalgesia, the research team scanned her DNA along with samples taken from her mother and two children. The team discovered two genetic changes: (1) mutations to the FAAH gene that reduced its expression, and (2) deletion of part of the FAAH pseudogene.

    The FAAH gene encodes for a protein called fatty acid amide hydrolase (FAAH). This protein breaks down fatty acid amides. Some of these compounds interact with cannabinoid receptors. These receptors are located in the membranes of cells found in tissues throughout the body. They mediate pain sensation, among other things. When fatty acid amide concentrations become elevated in the circulatory system, it produces an analgesic effect.

    Researchers found elevated fatty acid amide levels in the patient’s blood, consistent with reduced expression of the FAAH gene. It appears that both mutations are required for the complete hypoalgesia observed in the patient. The patient’s mother, daughter, and son all display only partial hypoalgesia. The mother and daughter have the same mutation in the FAAH gene but an intact FAAH pseudogene. The patient’s son is missing the FAAH pseudogene, but has a “normal” FAAH gene.

    Based on the data, it looks like proper expression levels of the FAAH gene require an intact FAAH pseudogene. This is not the first time that biomedical researchers have observed the same effect. There are a number of gene-pseudogene pairs in which both must be intact and transcribed for the gene to be expressed properly. In 2011, researchers from Harvard University proposed that the competitive endogenous RNA hypothesis explains why transcribed pseudogenes are so important for gene expression.2

    The Competitive Endogenous RNA Hypothesis

    Biochemists and molecular biologists have long believed that the primary mechanism for regulating gene expression centered around controlling the frequency and amount of mRNA produced during transcription. For housekeeping genes, mRNA is produced continually, while for genes that specify situational proteins, it is produced as needed. Greater amounts of mRNA are produced for genes expressed at high levels and limited amounts for genes expressed at low levels.

    Researchers long thought that once the mRNA was produced it would be translated into proteins, but recent discoveries indicate this is not the case. Instead, an elaborate mechanism exists that selectively degrades mRNA transcripts before they can be used to direct the protein production at the ribosome. This mechanism dictates the amount of protein produced by permitting or preventing mRNA from being translated. The selective degradation of mRNA also plays a role in gene expression, functioning in a complementary manner to the transcriptional control of gene expression.

    Another class of RNA molecules, called microRNAs, mediates the selective degradation of mRNA. In the early 2000s, biochemists recognized that by binding to mRNA (in the 3′ untranslated region of the transcript), microRNAs play a crucial role in gene regulation. Through binding, microRNAs flag the mRNA for destruction by RNA-induced silencing complex (RISC).

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    Figure 2: Schematic of the RNA-Induced Silencing Mechanism. Image Credit: Wikipedia

    Various distinct microRNA species in the cell bind to specific sites in the 3′ untranslated region of mRNA transcripts. (These binding locations are called microRNA response elements.) The selective binding by the population of microRNAs explains the role that duplicated pseudogenes play in regulating gene expression.

    The sequence similarity between the duplicated pseudogene and the corresponding “intact” gene means that the same microRNAs will bind to both mRNA transcripts. (It is interesting to note that most duplicated pseudogenes are transcribed.) When microRNAs bind to the transcript of the duplicated pseudogene, it allows the transcript of the “intact” gene to escape degradation. In other words, the transcript of the duplicated pseudogene is a decoy. The mRNA transcript can then be translated and, hence, the “intact” gene expressed.

    It is not just “intact” and duplicated pseudogenes that harbor the same microRNA response elements. Other genes share the same set of microRNA response elements in the 3′ untranslated region of the transcripts and, consequently, will bind the same set of microRNAs. These genes form a network that, when transcribed, will influence the expression of all genes in the network. This relationship means that all the mRNA transcripts in the network can function as decoys. This recognition accounts for the functional utility of unitary pseudogenes.

    One important consequence of this hypothesis is that mRNA has dual functions inside the cell. First, it encodes information needed to make proteins. Second, it helps regulate the expression of other transcripts that are part of its network.

    Junk DNA and the Case for Creation

    Evolutionary biologists have long maintained that identical (or nearly identical) pseudogene sequences found in corresponding locations in genomes of organisms that naturally group together (such as humans and the great apes) provide compelling evidence for shared ancestry. This interpretation was persuasive because molecular geneticists regarded pseudogenes as nonfunctional, junk DNA. Presumably, random biochemical events transformed functional DNA sequences (genes) into nonfunctional garbage.

    Creationists and intelligent design proponents had little to offer by way of evidence for the intentional design of genomes. But all this changed with the discovery that virtually every class of junk DNA has function, including all three types of pseudogenes (processed, duplicated, and unitary).

    If junk DNA is functional, then the sequences previously thought to show common descent could be understood as shared designs. The competitive endogenous RNA hypothesis supports this interpretation. This model provides an elegant rationale for the structural similarity between gene-pseudogene pairs and also makes sense of the widespread presence of unitary pseudogenes in genomes.

    Of course, this insight also supports the RTB genomics model. And that sure feels good to me.

    Resources

    Endnotes
    1. Abdella M. Habib et al., “Microdeletion in a FAAH Pseudogene Identified in a Patient with High Anandamide Concentrations and Pain Insensitivity,” British Journal of Anaesthesia, advanced access publication, doi:10.1016/j.bja.2019.02.019.
    2. Ana C. Marques, Jennifer Tan, and Chris P. Ponting, “Wrangling for microRNAs Provokes Much Crosstalk,” Genome Biology 12, no. 11 (November 2011): 132, doi:10.1186/gb-2011-12-11-132; Leonardo Salmena et al., “A ceRNA Hypothesis: The Rosetta Stone of a Hidden RNA Language?”, Cell 146, no. 3 (August 5, 2011): 353–58, doi:10.1016/j.cell.2011.07.014.
  • Why Mitochondria Make My List of Best Biological Designs

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | May 01, 2019

    A few days ago, I ran across a BuzzFeed list that catalogs 24 of the most poorly designed things in our time. Some of the items that stood out from the list for me were:

    • serial-wired Christmas lights
    • economy airplane seats
    • clamshell packaging
    • juice cartons
    • motion sensor faucets
    • jewel CD packaging
    • umbrellas

    What were people thinking when they designed these things? It’s difficult to argue with BuzzFeed’s list, though I bet you might add a few things of your own to their list of poor designs.

    If biologists were to make a list of poorly designed things, many would probably include…everything in biology. Most life scientists are influenced by an evolutionary perspective. Thus, they view biological systems as inherently flawed vestiges cobbled together by a set of historically contingent mechanisms.

    Yet as our understanding of biological systems improves, evidence shows that many “poorly designed” systems are actually exquisitely assembled. It also becomes evident that many biological designs reflect an impeccable logic that explains why these systems are the way they are. In other words, advances in biology reveal that it makes better sense to attribute biological systems to the work of a Mind, not to unguided evolution.

    Based on recent insights by biochemist and origin-of-life researcher Nick Lane, I would add mitochondria to my list of well-designed biological systems. Lane argues that complex cells and, ultimately, multicellular organisms would be impossible if it weren’t for mitochondria.1 (These organelles generate most of the ATP molecules used to power the operations of eukaryotic cells.) Toward this end, Lane has demonstrated that mitochondria’s properties are just-right for making complex eukaryotic cells possible. Without mitochondria, life would be limited to prokaryotic cells (bacteria and archaea).

    To put it another way, Nick Lane has shown that prokaryotic cells could never evolve the complexity needed to form cells with complexity akin to the eukaryotic cells required for multicellular organisms. The reason has to do with bioenergetic constraints placed on prokaryotic cells. According to Lane, the advent of mitochondria allowed life to break free from these constraints, paving the way for complex life.

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    Figure 1: A Mitochondrion. Image credit: Shutterstock

    Through Lane’s discovery, mitochondria reveal exquisite design and logical architecture and operations. Yet this is not necessarily what I (or many others) would have expected if mitochondria were the result of evolution. Rather, we’d expect biological systems to appear haphazard and purposeless, just good enough for the organism to survive and nothing more.

    To understand why I (and many evolutionary biologists) would hold this view about mitochondria and eukaryotic cells (assuming that they were the product of evolutionary processes), it is necessary to review the current evolutionary explanation for their origins.

    The Endosymbiont Hypothesis

    Most biologists believe that the endosymbiont hypothesis is the best explanation for the origin of complex eukaryotic cells. This hypothesis states that complex cells originated when single-celled microbes formed symbiotic relationships. “Host” microbes (most likely archaea) engulfed other archaea and/or bacteria, which then existed inside the host as endosymbionts.

    The presumption, then, is that organelles, including mitochondria, were once endosymbionts. Evolutionary biologists believe that, once engulfed, the endosymbionts took up permanent residency within the host cell and even grew and divided inside the host. Over time, the endosymbionts and the host became mutually interdependent. For example, the endosymbionts provided a metabolic benefit for the host cell, such as serving as a source of ATP. In turn, the host cell provided nutrients to the endosymbionts. The endosymbionts gradually evolved into organelles through a process referred to as genome reduction. This reduction resulted when genes from the endosymbionts’ genomes were transferred into the genome of the host organism.

    Based on this scenario, there is no real rationale for the existence of mitochondria (and eukaryotic cells). They are the way they are because they just wound up that way.

    But Nick Lane’s insights suggest otherwise.

    Lane’s analysis identifies a deep-seated rationale that accounts for the features of mitochondria (and eukaryotic cells) related to their contribution to cellular bioenergetics. To understand why mitochondria and eukaryotic cells are the way they are, we first need to understand why prokaryotic cells can never evolve into large complex cells, a necessary step for the advent of complex multicellular organisms.

    Bioenergetics Constraints on Prokaryotic Cells

    Lane has discovered that bioenergetics constraints keep bacterial and archaeal cells trapped at their current size and complexity. Key to discovering this constraint is a metric Lane devised called Available Energy per Gene (AEG). It turns out that AEG in eukaryotic cells can be as much as 200,000 times larger than the AEG in prokaryotic cells. This extra energy allows eukaryotic cells to engage in a wide range of metabolic processes that support cellular complexity. Prokaryotic cells simply can’t afford such processes.

    An average eukaryotic cell has between 20,000 to 40,000 genes; a typical bacterial cell has about 5,000 genes. Each gene encodes the information the cell’s machinery needs to make a distinct protein. And proteins are the workhorse molecules of the cell. More genes mean a more diverse suite of proteins, which means greater biochemical complexity.

    So, what is so special about eukaryotic cells? Why don’t prokaryotic cells have the same AEG? Why do eukaryotic cells have an expanded repertoire of genes and prokaryotic cells don’t?

    In short, the answer is: mitochondria.

    On average, the volume of eukaryotic cells is about 15,000 times larger than that of prokaryotic cells. Eukaryotic cells’ larger size allows for their greater complexity. Lane estimates that for a prokaryotic cell to scale up to this volume, its radius would need to increase 25-fold and its surface area 625-fold.

    Because the plasma membrane of bacteria is the site for ATP synthesis, increases in the surface area would allow the hypothetically enlarged bacteria to produce 625 times more ATP. But this increased ATP production doesn’t increase the AEG. Why is that?

    The bacteria would have to produce 625 times more proteins to support the increased ATP production. Because the cell’s machinery must access the bacteria’s DNA to make these proteins, a single copy of the genome is insufficient to support all of the activity centered around the synthesis of that many proteins. In fact, Lane estimates that for bacteria to increase its ATP production 625-fold, it would require 625 copies of its genome. In other words, even though the bacteria increased in size, in effect, the AEG remains unchanged.

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    Figure 2: ATP Production at the Cell Membrane Surface. Image credit: Shutterstock

    Things become more complicated when factoring in cell volume. When the surface area (and concomitant ATP production) increase by a factor of 625, the volume of the cell expands 15,000 times. To satisfy the demands of a larger cell, even more copies of the genome would be required, perhaps as many as 15,000. But energy production tops off at a 625-fold increase. This mismatch means that the AEG drops by 25 percent per gene. For a genome consisting of 5,000 genes, this drop means that a bacterium the size of a eukaryotic cell would have about 125,000 times less AEG than a typical eukaryotic cell and 200,000 times less AEG when compared to eukaryotes with genome sizes approaching 40,000 genes.

    Bioenergetic Freedom for Eukaryotic Cells

    Thanks to mitochondria, eukaryotic cells are free from the bioenergetic constraints that ensnare prokaryotic cells. Mitochondria generate the same amount of ATP as a bacterial cell. However, their genome consists of only 13 proteins, thus the organelle’s ATP demand is low. The net effect is that the mitochondria’s AEG skyrockets. Furthermore, mitochondrial membranes come equipped with an ATP transport protein that can pump the vast excess of ATP from the organelle interior into the cytoplasm for the eukaryotic cell to use.

    To summarize, mitochondria’s small genome plus its prodigious ATP output are the keys to eukaryotic cells’ large AEG.

    Of course, this raises a question: Why do mitochondria have genomes at all? Well, as it turns out, mitochondria need genomes for several reasons (which I’ve detailed in previous articles).

    Other features of mitochondria are also essential for ATP production. For example, cardiolipin in the organelle’s inner membrane plays a role in stabilizing and organizing specific proteins needed for cellular energy production.

    From a creation perspective it seems that if a Creator was going to design a eukaryotic cell from scratch, he would have to create an organelle just like a mitochondrion to provide the energy needed to sustain the cell’s complexity with a high AEG. Far from being an evolutionary “kludge job,” mitochondria appear to be an elegantly designed feature of eukaryotic cells with a just-right set of properties that allow for the cellular complexity needed to sustain complex multicellular life. It is eerie to think that unguided evolutionary events just happened to traverse the just-right evolutionary path to yield such an organelle.

    As a Christian, I see the rationale that undergirds the design of mitochondria as the signature of the Creator’s handiwork in biology. I also view the anthropic coincidence associated with the origin of eukaryotic cells as reason to believe that life’s history has purpose and meaning, pointing toward the advent of complex life and humanity.

    So, now you know why mitochondria make my list.

    Resources

    Endnotes
    1. Nick Lane, “Bioenergetic Constraints on the Evolution of Complex Life,” Cold Spring Harbor Perspectives in Biology 6, no. 5 (May 2014): a015982, doi:10.1101/cshperspect.a015982.
  • Self-Assembly of Protein Machines: Evidence for Evolution or Creation?

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | Apr 17, 2019

    I finally upgraded my iPhone a few weeks ago from a 5s to an 8 Plus. I had little choice. The battery on my cell phone would no longer hold a charge.

    I’d put off getting a new one for as long as possible. It just didn’t make sense to spend money chasing the latest and greatest technology when current cell phone technology worked perfectly fine for me. Apart from the battery life and a less-than-ideal camera, I was happy with my iPhone 5s. Now I am really glad I made the switch.

    Then, the other day I caught myself wistfully eyeing the iPhone X. And, today, I learned that Apple is preparing the release of the iPhone 11 (or XI or XT). Where will Apple’s technology upgrades take us next? I can’t wait to find out.

    Have I become a technology junkie?

    It is remarkable how quickly cell phone technology advances. It is also remarkable how alluring new technology can be. The next thing you know, Apple will release an iPhone that will assemble itself when it comes out of the box. . . . Probably not.

    But, if the work of engineers at MIT ever reaches fruition, it is possible that smartphone manufacturers one day just might rely on a self-assembly process to produce cell phones.

    A Self-Assembling Cell Phone

    The Self-Assembly Lab at MIT has developed a pilot process to manufacture cell phones by self-assembly.

    To do this, they designed their cell phone to consist of six parts that fit together in a lock-in-key manner. By placing the cell phone pieces into a tumbler that turns at the just-right speed, the pieces automatically combine with one another, bit by bit, until the cell phone is assembled.

    Few errors occur during the assembly process. Only pieces designed to fit together combine with one another because of the lock-in-key fabrication.

    Self-Assembly and the Case for a Creator

    It is quite likely that the work of MIT’s Self-Assembly Lab (and other labs like it) will one day revolutionize manufacturing—not just for iPhones, but for other types of products as well.

    As alluring as this new technology might be, I am more intrigued by its implications for the creation-evolution controversy. What do self-assembly processes have to do with the creation-evolution debate? More than we might realize.

    I believe self-assembly processes strengthen the watchmaker argument for God’s existence (and role in the origin of life). Namely, this cutting-edge technology makes it possible to respond to a common objection leveled against this design argument.

    To understand why this engineering breakthrough is so important for the Watchmaker argument, a little background is necessary.

    The Watchmaker Argument

    Anglican natural theologian William Paley (1743–1805) posited the Watchmaker argument in the eighteenth century. It went on to become one of the best-known arguments for God’s existence. The argument hinges on the comparison Paley made between a watch and a rock. He argued that a rock’s existence can be explained by the outworking of natural processes—not so for a watch.

    The characteristics of a watch—specifically the complex interaction of its precision parts for the purpose of telling time—implied the work of an intelligent designer. Employing an analogy, Paley asserted that just as a watch requires a watchmaker, so too, life requires a Creator. Paley noted that biological systems display a wide range of features characterized by the precise interplay of complex parts designed to interact for specific purposes. In other words, biological systems have much more in common with a watch than a rock. This similarity being the case, it logically follows that life must stem from the work of a Divine Watchmaker.

    Biochemistry and the Watchmaker Argument

    As I discuss in my book The Cell’s Design, advances in biochemistry have reinvigorated the Watchmaker argument. The hallmark features of biochemical systems are precisely the same properties displayed in objects, devices, and systems designed and crafted by humans.

    Cells contain protein complexes that are structured to operate as biomolecular motors and machines. Some molecular-level biomachines are strict analogs to machinery produced by human designers. In fact, in many instances, a one-to-one relationship exists between the parts of manufactured machines and the molecular components of biomachines. (A few examples of these biomolecular machines are discussed in the articles listed in the Resources section.)

    We know that machines originate in human minds that comprehend and then implement designs. So, when scientists discover example after example of biomolecular machines inside the cell with an eerie and startling similarity to the machines we produce, it makes sense to conclude that these machines and, hence, life, must also have originated in a Mind.

    A Skeptic’s Challenge

    As you might imagine, skeptics have leveled objections against the Watchmaker argument since its introduction in the 1700s. Today, when skeptics criticize the latest version of the Watchmaker argument (based on biochemical designs), the influence of Scottish skeptic David Hume (1711–1776) can be seen and felt.

    In his 1779 work Dialogues Concerning Natural Religion, Hume presented several criticisms of design arguments. The foremost centered on the nature of analogical reasoning. Hume argued that the conclusions resulting from analogical reasoning are only sound when the things compared are highly similar to each other. The more similar, the stronger the conclusion. The less similar, the weaker the conclusion.

    Hume dismissed the original version of the Watchmaker argument by maintaining that organisms and watches are nothing alike. They are too dissimilar for a good analogy. In other words, what is true for a watch is not necessarily true for an organism and, therefore, it doesn’t follow that organisms require a Divine Watchmaker, just because a watch does.

    In effect, this is one of the chief reasons why some skeptics today dismiss the biochemical Watchmaker argument. For example, philosopher Massimo Pigliucci has insisted that Paley’s analogy is purely metaphorical and does not reflect a true analogical relationship. He maintains that any similarity between biomolecular machines and human designs reflects merely illustrative analogies that life scientists use to communicate the structure and function of these protein complexes via familiar concepts and language. In other words, it is illegitimate to use the “analogies” between biomolecular machines and manufactured machines to make a case for a Creator.1

    A Response Based on Insights from Nanotechnology

    I have responded to this objection by pointing out that nanotechnologists have isolated biomolecular machines from the cell and incorporated these protein complexes into nanodevices and nanosystems for the explicit purpose of taking advantage of their machine-like properties. These transplanted biomachines power motion and movements in the devices, which otherwise would be impossible with current technology. In other words, nanotechnologists view these biomolecular systems as actual machines and utilize them as such. Their work demonstrates that biomolecular machines are literal, not metaphorical, machines. (See the Resources section for articles describing this work.)

    Is Self-Assembly Evidence of Evolution or Design?

    Another criticism—inspired by Hume—is that machines designed by humans don’t self-assemble, but biochemical machines do. Skeptics say this undermines the Watchmaker analogy. I have heard this criticism in the past, but it came up recently in a dialogue I had with a skeptic in a Facebook group.

    I wrote that “What we discover when we work out the structure and function of protein complexes are features that are akin to an automobile engine, not an outcropping of rocks.”

    A skeptic named Maurice responded: “Your analogy is false. Cars do not spontaneously self-assemble—in that case there is a prohibitive energy barrier. But hexagonal lava rocks can and do—there is no energy barrier to prohibit that from happening.”

    Maurice argues that my analogy is a poor one because protein complexes in the cell self-assemble, whereas automobile engines can’t. For Maurice (and other skeptics), this distinction serves to make manufactured machines qualitatively different from biomolecular machines. On the other hand, hexagonal patterns in lava rocks give the appearance of design but are actually formed spontaneously. For skeptics like Maurice, this feature indicates that the design displayed by protein complexes in the cell is apparent, not true, design.

    Maurice added: “Given that nature can make hexagonal lava blocks look ‘designed,’ it can certainly make other objects look ‘designed.’ Design is not a scientific term.”

    Self-Assembly and the Watchmaker Argument

    This is where the MIT engineers’ fascinating work comes into play.

    Engineers continue to make significant progress toward developing self-assembly processes for manufacturing purposes. It very well could be that in the future a number of machines and devices will be designed to self-assemble. Based on the researchers’ work, it becomes evident that part of the strategy for designing machines that self-assemble centers on creating components that not only contribute to the machine’s function, but also precisely interact with the other components so that the machine assembles on its own.

    The operative word here is designed. For machines to self-assemble they must be designed to self-assemble.

    This requirement holds true for biochemical machines, too. The protein subunits that interact to form the biomolecular machines appear to be designed for self-assembly. Protein-protein binding sites on the surface of the subunits mediate this self-assembly process. These binding sites require high-precision interactions to ensure that the binding between subunits takes place with a high degree of accuracy—in the same way that the MIT engineers designed the cell phone pieces to precisely combine through lock-in-key interactions.

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    Figure: ATP Synthase is a biomolecular motor that is literally an electrically powered rotary motor. This biomachine is assembled from protein subunits. Credit: Shutterstock

    The level of design required to ensure that protein subunits interact precisely to form machine-like protein complexes is only beginning to come into full view.2 Biochemists who work in the area of protein design still don’t fully understand the biophysical mechanisms that dictate the assembly of protein subunits. And, while they can design proteins that will self-assemble, they struggle to replicate the complexity of the self-assembly process that routinely takes place inside the cell.

    Thanks to advances in technology, biomolecular machines’ ability to self-assemble should no longer count against the Watchmaker argument. Instead, self-assembly becomes one more feature that strengthens Paley’s point.

    The Watchmaker Prediction

    Advances in self-assembly also satisfy the Watchmaker prediction, further strengthening the case for a Creator. In conjunction with my presentation of the revitalized Watchmaker argument in The Cell’s Design, I proposed the Watchmaker prediction. I contend that many of the cell’s molecular systems currently go unrecognized as analogs to human designs because the corresponding technology has yet to be developed.

    The possibility that advances in human technology will ultimately mirror the molecular technology that already exists as an integral part of biochemical systems leads to the Watchmaker prediction. As human designers develop new technologies, examples of these technologies, though previously unrecognized, will become evident in the operation of the cell’s molecular systems. In other words, if the Watchmaker argument truly serves as evidence for a Creator’s existence, then it is reasonable to expect that life’s biochemical machinery anticipates human technological advances.

    In effect, the developments in self-assembly technology and its prospective use in future manufacturing operations fulfill the Watchmaker prediction. Along these lines, it’s even more provocative to think that cellular self-assembly processes are providing insight to engineers who are working to develop similar technology.

    Maybe I am a technology junkie, after all. I find it remarkable that as we develop new technologies we discover that they already exist in the cell, and because they do the Watchmaker argument becomes more and more compelling.

    Can you hear me now?

    Resources

    The Biochemical Watchmaker Argument

    Challenges to the Biochemical Watchmaker Argument

    Endnotes
    1. Massimo Pigliucci and Maarten Boudry, “Why Machine-Information Metaphors are Bad for Science and Science Education,” Science and Education 20, no. 5–6 (May 2011): 453–71; doi:10.1007/s11191-010-9267-6.
    2. For example, see Christoffer H. Norn and Ingemar André, “Computational Design of Protein Self-Assembly,” Current Opinion in Structural Biology 39 (August 2016): 39–45, doi:10.1016/j.sbi.2016.04.002.
  • Does Transhumanism Refute Human Exceptionalism? A Response to Peter Clarke

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | Apr 03, 2019

    I just finished binge-watching Altered Carbon. Based on the 2002 science fiction novel written by Richard K. Morgan, this Netflix original series is provocative, to say the least.

    Altered Carbon takes place in the future, where humans can store their personalities as digital files in devices called stacks. These disc-like devices are implanted at the top of the spinal column. When people die, their stacks can be removed from their body (called sleeves) and stored indefinitely until they are re-sleeved—if and when another body becomes available to them.

    In this world, people who possess extreme wealth can live indefinitely, without ever having to spend any time in storage. Referred to as Meths (after the biblical figure Methuselah, who lived 969 years), the wealthy have the financial resources to secure a continual supply of replacement bodies through cloning. Their wealth also affords them the means to back up their stacks once a day, storing the data in a remote location in case their stacks are destroyed. In effect, Meths use technology to attain a form of immortality.

    Forthcoming Posthuman Reality?

    The world of Altered Carbon is becoming a reality right before our eyes. Thanks to recent advances in biotechnology and bioengineering, the idea of using technology to help people live indefinitely no longer falls under the purview of science fiction. Emerging technologies such as CRISPR-Cas9 gene editing and brain-computer interfaces offer hope to people suffering from debilitating diseases and injuries. They can also be used for human enhancements—extending our physical, intellectual, and psychological capabilities beyond natural biological limits.

    These futuristic possibilities give fuel to a movement known as transhumanism. Residing on the fringe of the academy and culture for several decades, the movement has gone mainstream in the ivory towers of the academy and on the street. Sociologist James Hughes describes the transhumanist vision this way in his book Citizen Cyborg:

    “In the twenty-first century the convergence of artificial intelligence, nanotechnology and genetic engineering will allow human beings to achieve things previously imagined only in science fiction. Lifespans will extend well beyond a century. Our senses and cognition will be enhanced. We will gain control over our emotions and memory. We will merge with machines, and machines will become more like humans. These technologies will allow us to evolve into varieties of “posthumans” and usher us into a “transhuman” era and society. . . . Transhuman technologies, technologies that push the boundaries of humanism, can radically improve our quality of life, and . . . we have a fundamental right to use them to control our bodies and minds. But to ensure these benefits we need to democratically regulate these technologies and make them equally available in free societies.”1

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    Figure 1: The transhumanism symbol. Image credit: Wikimedia Commons

    In short, transhumanists want us to take control of our own evolution, transforming human beings into posthumans and in the process creating a utopian future that carves out a path to immortality.

    Depending on one’s philosophical or religious perspective, transhumanists’ vision and the prospects of a posthuman reality can bring excitement or concern or a little bit of both. Should we pursue the use of technology to enhance ourselves, transcending the constraints of our biology? What role should these emerging biotechnologies play in shaping our future? What are the boundaries for developing and using these technologies? Should there be any boundaries?2

    All of these questions revolve around a central question: Who are we as human beings?

    Are Humans Exceptional?

    Prior to the rising influence of transhumanism, the answer to this question followed along one of two lines. For people who hold to a Judeo-Christian worldview, human beings are exceptional, standing apart from all other creatures on the planet. Accordingly, our exceptional nature results from the image of God. As image bearers, human beings have infinite worth and value.

    On the other hand, those influenced by the evolutionary paradigm maintain that human beings are nothing more than animals—differing in degree, not kind, from other creatures. In fact, many who hold this view of humanity find the notion of human exceptionalism repugnant. In their view, to elevate the value of human beings above that of other creatures constitutes speciesism and reflects an unjustifiable arrogance.

    And now transhumanism enters into the fray. People on both sides of the controversy about human nature and identity argue that transhumanism brings an end to any notion about human exceptionalism, once and for all.

    One is Peter Clarke. In an article published on the Areo website entitled “Transhumanism and the Death of Human Exceptionalism,” Clarke says:

    “As a philosophical movement, transhumanism advocates for improving humanity through genetic modifications and technological augmentations, based upon the position that there is nothing particularly sacred about the human condition. It acknowledges up front that our bodies and minds are riddled with flaws that not only can but should be fixed. Even more radically, as the name implies, transhumanism embraces the potential of one day moving beyond the human condition, transitioning our sentience into more advanced forms of life, including genetically modified humans, superhuman cyborgs, and immortal digital intelligences.”3

    On the other side of the aisle is Wesley J. Smith of the Discovery Institute. In his article “Transhumanist Bill of Wrongs,” Smith writes:

    “Transhumanism would shatter human exceptionalism. The moral philosophy of the West holds that each human being is possessed of natural rights that adhere solely and merely because we are human. But transhumanists yearn to remake humanity in their own image—including as cyborgs, group personalities residing in the Internet Cloud, or AI-controlled machines. That requires denigrating natural man as unexceptional to justify our substantial deconstruction and redesign.”4

    In other words, transhumanism highlights the notion that our bodies, minds, and personalities are inherently flawed and we have a moral imperative, proponents say, to correct these flaws. But this view denigrates humanity, opponents say, and with it the notion of human exceptionalism. For Clarke, this nonexceptional perspective is something to be celebrated. For Smith, transhumanism is of utmost concern and must be opposed.

    Evidence of Exceptionalism

    While I am sympathetic to Smith’s concern, I would take a differing perspective. I find that transhumanism provides one of the most powerful pieces of evidence for human exceptionalism—and along with it the image of God.

    In my forthcoming book (coauthored with Ken Samples), Humans 2.0, I write:

    “Ironically, progress in human enhancement technology and the prospects of a posthuman future serve as one of the most powerful arguments for human exceptionalism and, consequently, the image of God. Human beings are the only species that exists—or that has ever existed—that can create technologies to enhance our capabilities beyond our biological limits. We alone work toward effecting our own immortality, take control of evolution, and look to usher in a posthuman world. These possibilities stem from our unique and exceptional capacity to investigate and develop an understanding of nature (including human biology) through science and then turn that insight into technology.”5

    Our ability to carry out the scientific enterprise and develop technology stems from four qualities that a growing number of anthropologists and primatologists think are unique to humans, including:

    • symbolism
    • open-ended generative capacity
    • theory of mind
    • our capacity to form complex social networks

    From my perspective as a Christian, these qualities stand as scientific descriptors of the image of God.

    As human beings, we effortlessly represent the world with discrete symbols. We denote abstract concepts with symbols. And our ability to represent the world symbolically has interesting consequences when coupled with our abilities to combine and recombine those symbols in a nearly infinite number of ways to create alternate possibilities.

    Human capacity for symbolism manifests in the form of language, art, music, and even body ornamentation. And we desire to communicate the scenarios we construct in our minds with other human beings.

    For anthropologists and primatologists who think that human beings differ in kind—not degree—from other animals, these qualities demarcate us from the great apes and Neanderthals. The separation becomes most apparent when we consider the remarkable technological advances we have made during our tenure as a species. Primatologist Thomas Suddendorf puts it this way:

    “We reflect on and argue about our present situation, our history, and our destiny. We envision wonderful harmonious worlds as easily as we do dreadful tyrannies. Our powers are used for good as they are for bad, and we incessantly debate which is which. Our minds have spawned civilizations and technologies that have changed the face of the Earth, while our closest living animal relatives sit unobtrusively in their remaining forests. There appears to be a tremendous gap between human and animal minds.”6

    Moreover, no convincing evidence exists that leads us to think that Neanderthals shared the qualities that make us exceptional. Neanderthals—who first appear in the fossil record around 250,000 to 200,000 years ago and disappear around 40,000 years ago—existed on Earth longer than modern humans have. Yet our technology has progressed exponentially, while Neanderthal technology remained largely static.

    According to paleoanthropologist Ian Tattersall and linguist Noam Chomsky (and their coauthors):

    “Our species was born in a technologically archaic context, and significantly, the tempo of change only began picking up after the point at which symbolic objects appeared. Evidently, a new potential for symbolic thought was born with our anatomically distinctive species, but it was only expressed after a necessary cultural stimulus had exerted itself. This stimulus was most plausibly the appearance of language. . . . Then, within a remarkably short space of time, art was invented, cities were born, and people had reached the moon.”7

    In other words, the evolution of human technology signifies that there is something special—exceptional—about us as human beings. In this sense, transhumanism highlights our exceptional nature precisely because the prospects for controlling our own evolution stem from our ability to advance technology.

    To be clear, transhumanism possesses an existential risk for humanity. Unquestioningly, it has the potential to strip human beings of dignity and worth. But, ironically, transhumanism is possible only because we are exceptional as human beings.

    Responsibility as the Crown of Creation

    Ultimately, our exceptional nature demands that we thoughtfully deliberate on how to use emerging biotechnologies to promote human flourishing, while ensuring that no human being is exploited or marginalized by these technologies. It also means that we must preserve our identity as human beings at all costs.

    It is one thing to enjoy contemplating a posthuman future by binge-watching a sci-fi TV series. But, it is another thing altogether to live it out. May we be guided by ethical wisdom to live well.

    Resources

    Endnotes
    1. James Hughes, Citizen Cyborg: Why Democratic Societies Must Respond to the Redesigned Humans of the Future (Cambridge, MA: Westview Press, 2004), xii.
    2. Ken Samples and I take on these questions and more in our book Humans 2.0, due to be published in July of 2019.
    3. Peter Clarke, Transhumanism and the Death of Human Exceptionalism, Areo (March 6, 2019), https://areomagazine.com/2019/03/06/transhumanism-and-the-death-of-human-exceptionalism/.
    4. Wesley J. Smith,Transhumanist Bill of Wrongs, Discovery Institute (October 23, 2018), https://www.discovery.org/a/transhumanist-bill-of-wrongs/.
    5. Fazale Rana with Kenneth Samples, Humans 2.0: Scientific, Philosophical, and Theological Perspectives on Transhumanism (Covina, CA: RTB Press, 2019) in press.
    6. Thomas Suddendorf, The Gap: The Science of What Separates Us from Other Animals (New York: Basic Books, 2013), 2.
    7. Johan J. Bolhuis et al., “How Could Language Have Evolved?” PLoS Biology 12, no.8 (August 26, 2014): e1001934, doi:10.1371/journal.pbio.1001934.
  • Timing of Neanderthals’ Disappearance Makes Art Claims Unlikely

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | Mar 27, 2019

    In Latin it literally means, “somewhere else.”

    Legal experts consider an alibi to be one of the most effective legal defenses available in a court of law because it has the potential to prove a defendant’s innocence. It goes without saying: if a defendant has an alibi, it means that he or she was somewhere else when the crime was committed.

    As it turns out, paleoanthropologists have discovered that Neanderthals have an alibi, of sorts. Evidence indicates that they weren’t the ones to scratch up the floor of Gorham’s Cave.

    Based on recent radiocarbon dates measured for samples from Bajondillo Cave (located on the southern part of the Iberian Peninsula—southwest corner of Europe), a research team from the Japan Agency for Marine-Earth Science and Technology and several Spanish institutions determined that modern humans made their way to the southernmost tip of Iberia around 43,000 years ago, displacing Neanderthals.1

    Because Neanderthals disappeared from Iberia at that time, it becomes unlikely that they were responsible for hatch marks (dated to be 39,000 years in age) made on the floor of Gorham’s Cave on the island of Gibraltar. These scratches have been interpreted by some paleoanthropologists as evidence that Neanderthals possessed symbolic capabilities.

    But how could Neanderthals have made the hatch marks if they weren’t there? Ladies and gentlemen of the jury: the perfect alibi. Instead, it looks as if modern humans were the culprits who marked up the cave floor.

    blog__inline--timing-of-neanderthals-disappearance-1

    Figure 1: Gorham’s Cave. Image credit: Wikipedia

    The Case for Neanderthal Exceptionalism

    Two of the biggest questions in anthropology today relate to Neanderthals:

    • When did these creatures disappear from Europe?
    • Did they possess symbolic capacity like modern humans, thus putting their cognitive abilities on par with ours as a species?

    For paleoanthropologists, these two questions have become inseparable. With regard to the second question, some paleoanthropologists are convinced that Neanderthals displayed symbolic capabilities.

    It is important to note that the case for Neanderthal symbolism is largely based on correlations between the archaeological and fossil records. Toward this end, some anthropologists have concluded that Neanderthals possessed symbolism because researchers have recovered artifacts (presumably reflecting symbolic capabilities) from the same layers that harbored Neanderthal fossils. Unfortunately, this approach is complicated by other studies that show that the cave layers have been mixed by either cave occupants (either hominid or modern human) or animals living in the caves. This mixing leads to the accidental association of fossil and archaeological remains. In other words, the mixing of layers raises questions about who the manufacturers of these artifacts were.

    Because we know modern humans possess the capacity for symbolism, it is much more likely that modern humans, not Neanderthals, made the symbolic artifacts, in these instances. Then, only through an upheaval of the cave layers did the artifacts mix with Neanderthal remains. (See the Resources section for articles that elaborate this point.)

    More often than not, archaeological remains are unearthed by themselves with no corresponding fossil specimens. This is the reason why understanding the timing of Neanderthals disappearance and modern humans arrival in different regions of Europe becomes so important (and why the two questions interrelate). Paleoanthropologists believe that if they can show that Neanderthals lived in a locale at the time symbolic artifacts were produced, then it becomes conceivable that these creatures made the symbolic items. This interpretation increases in plausiblity if no modern humans were around at the time.

    Some researchers have argued along these lines regarding the hatch marks found on the floor of Gorham’s Cave.2 The markings were made in the bedrock of the cave floor. The layers above the bedrock date to between 30,000 and 39,000 years in age. Some paleoanthropologists argue that Neanderthals must have made the markings. Why? Because, even though modern humans were already in Europe by that time, these paleoanthropologists think that modern humans had not yet made their way to the southern part of the Iberian Peninsula. These same researchers also think that Neanderthals survived in Iberia until about 32,000 years ago, even though their counterparts in other parts of Europe had already disappeared. So, on this basis, paleoanthropologists conclude that Neanderthals produced the hatch marks and, thus, displayed symbolic capabilities.

    blog__inline--timing-of-neanderthals-disappearance-2

    Figure 2: Hatch marks on the floor of Gorham’s Cave. Image credit: Wikipedia

    When Did Neanderthals Disappear from Iberia?

    But recent work challenges this conclusion. The Spanish and Japanese team took 17 new radiocarbon measurements from layers of the Bajondillo Cave (located in southern Iberia, near Gorham’s Cave) with the hopes of precisely documenting the change in technology from Mousterian (made by Neanderthals) to Aurignacian (made by modern humans). This transition corresponds to the replacement of Neanderthals by modern humans elsewhere in Europe.

    The researchers combined the data from their samples with previous measurements made at the site to pinpoint this transition at around 43,000 years ago—not 32,000 years ago. In other words, modern humans occupied Iberia at the same time they occupied other places in Europe. This result also means that Neanderthals had disappeared from Iberia well before the hatch marks in Gorham’s Cave were made.

    Were Neanderthals Exceptional Like Modern Humans?

    Though claims of Neanderthal exceptionalism abound in the scientific literature and in popular science articles, the claims universally fail to withstand ongoing scientific scrutiny, as this latest discovery attests. Simply put, based on the archaeological record, there are no good reasons to think that Neanderthals displayed symbolism.

    From my perspective, the case for Neanderthal symbolism seems to be driven more by ideology than actual scientific evidence.

    It is also worth noting that comparative studies on Neanderthal and modern human brain structures also lead to the conclusion that humans displayed symbolism and Neanderthals did not. (See the Resources section for articles that describe this work in more detail.)

    Why Does It Matter?

    Questions about Neanderthal symbolic capacity and, hence, exceptionalism have bearing on how we understand human beings. Are human beings unique in our capacity for symbolism or is this quality displayed by other hominins? If humans are not alone in our capacity for symbolism, then we aren’t exceptional. And, if we aren’t exceptional then it becomes untenable to embrace the biblical concept of human beings as God’s image bearers. (As a Christian, I see symbolism as a manifestation of the image of God.)

    But, based on the latest scientific evidence, the verdict is in: modern humans are the only species to display the capacity for symbolism. In this way, scientific advance affirms that humans are exceptional in a way that aligns with the biblical concept of the image of God.

    The Neanderthals alibi holds up. They werent there, but humans were. Case closed.

    Resources

    Endnotes
    1. Miguel Cortés-Sánchez et al., “An Early Aurignacian Arrival in Southwestern Europe,” Nature Ecology and Evolution 3 (January 21, 2019): 207–12, doi:10.1038/s41559-018-0753-6.
    2. Joaquín Rodríguez-Vidal et al., “A Rock Engraving Made by Neanderthals in Gibraltar,” Proceedings of the National Academy of Sciences USA 111, no. 37 (September 16, 2014): 13301–6, doi:10.1073/pnas.1411529111.
  • Origins of Monogamy Cause Evolutionary Paradigm Breakup

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | Mar 20, 2019

    Gregg Allman fronted the Allman Brothers Band for over 40 years until his death in 2017 at the age of 69. Writer Mark Binelli described Allman’s voice as “a beautifully scarred blues howl, old beyond its years.”1

    A rock legend who helped pioneer southern rock, Allman was as well known for his chaotic, dysfunctional personal life as for his accomplishments as a musician. Allman struggled with drug abuse and addiction. He was also married six times, with each marriage ending in divorce and, at times, in a public spectacle.

    In a 2009 interview with Binelli for Rolling Stone, Allman reflected on his failed marriages: “To tell you the truth, it’s my sixth marriage—I’m starting to think it’s me.”2

    Allman isn’t the only one to have trouble with marriage. As it turns out, so do evolutionary biologists—but for different reasons than Greg Allman.

    To be more exact, evolutionary biologists have made an unexpected discovery about the evolutionary origin of monogamy (a single mate for at least a season) in animals—an insight that raises questions about the evolutionary explanation. Based on recent work headed by a large research team of investigators from the University of Texas (UT), Austin, it looks like monogamy arose independently, multiple times, in animals. And these origin events were driven, in each instance, by the same genetic changes.3

    In my view, this remarkable example of evolutionary convergence highlights one of the many limitations of evolutionary theory. It also contributes to my skepticism (and that of other intelligent design proponents/creationists) about the central claim of the evolutionary paradigm; namely, the origin, design, history, and diversity of life can be fully explained by evolutionary mechanisms.

    At the same time, the independent origins of monogamy—driven by the same genetic changes—(as well as other examples of convergence) find a ready explanation within a creation model framework.

    Historical Contingency

    To appreciate why I believe this discovery is problematic for the evolutionary paradigm, it is necessary to consider the nature of evolutionary mechanisms. According to the evolutionary biologist Stephen Jay Gould (1941–2002), evolutionary transformations occur in a historically contingent manner.4 This means that the evolutionary process consists of an extended sequence of unpredictable, chance events. If any of these events were altered, it would send evolution down a different trajectory.

    To help clarify this concept, Gould used the metaphor of “replaying life’s tape.” If one were to push the rewind button, erase life’s history, and then let the tape run again, the results would be completely different each time. In other words, the evolutionary process should not repeat itself. And rarely should it arrive at the same end point.

    Gould based the concept of historical contingency on his understanding of the mechanisms that drive evolutionary change. Since the time of Gould’s original description of historical contingency, several studies have affirmed his view. (For descriptions of some representative studies, see the articles listed in the Resources section.) In other words, researchers have experimentally shown that the evolutionary process is, indeed, historically contingent.

    A Failed Prediction of the Evolutionary Paradigm

    Given historical contingency, it seems unlikely that distinct evolutionary pathways would lead to identical or nearly identical outcomes. Yet, when viewed from an evolutionary standpoint, it appears as if repeated evolutionary outcomes are a common occurrence throughout life’s history. This phenomenon—referred to as convergence—is widespread. Evolutionary biologists Simon Conway Morris and George McGhee point out in their respective books, Life’s Solution and Convergent Evolution, that identical evolutionary outcomes are a characteristic feature of the biological realm.5 Scientists see these repeated outcomes at the ecological, organismal, biochemical, and genetic levels. In fact, in my book The Cell’s Design, I describe 100 examples of convergence at the biochemical level.

    In other words, biologists have made two contradictory observations within the evolutionary framework: (1) evolutionary processes are historically contingent and (2) evolutionary convergence is widespread. Since the publication of The Cell’s Design, many new examples of convergence have been unearthed, including the recent origin of monogamy discovery.

    Convergent Origins of Monogamy

    Working within the framework of the evolutionary paradigm, the UT research team sought to understand the evolutionary transition to monogamy. To achieve this insight, they compared the gene expression profiles in the neural tissues of reproductive males for closely related pairs of species, with one species displaying monogamous behavior and the other nonmonogamous reproduction.

    The species pairs spanned the major vertebrate groups and included mice, voles, songbirds, frogs, and cichlids. From an evolutionary perspective, these organisms would have shared a common ancestor 450 million years ago.

    Monogamous behavior is remarkably complex. It involves the formation of bonds between males and females, care of offspring by both parents, and increased territorial defense. Yet, the researchers discovered that in each instance of monogamy the gene expression profiles in the neural tissues of the monogamous species were identical and distinct from the gene expression patterns for their nonmonogamous counterparts. Specifically, they observed the same differences in gene expression for the same 24 genes. Interestingly, genes that played a role in neural development, cell-cell signaling, synaptic activity, learning and memory, and cognitive function displayed enhanced gene expression. Genes involved in gene transcription and AMPA receptor regulation were down-regulated.

    So, how do the researchers account for this spectacular example of convergence? They conclude that a “universal transcriptomic mechanism” exists for monogamy and speculate that the gene modules needed for monogamous behavior already existed in the last common ancestor of vertebrates. When needed, these modules were independently recruited at different times in evolutionary history to yield monogamous species.

    Yet, given the number of genes involved and the specific changes in gene expression needed to produce the complex behavior associated with monogamous reproduction, it seems unlikely that this transformation would happen a single time, let alone multiple times, in the exact same way. In fact, Rebecca Young, the lead author of the journal article detailing the UT research team’s work, notes that “Most people wouldn’t expect that across 450 million years, transitions to such complex behaviors would happen the same way every time.”6

    So, is there another way to explain convergence?

    Convergence and the Case for a Creator

    Prior to Darwin (1809–1882), biologists referred to shared biological features found in organisms that cluster into disparate biological groups as analogies. (In an evolutionary framework, analogies are referred to as evolutionary convergences.) They viewed analogous systems as designs conceived by the Creator that were then physically manifested in the biological realm and distributed among unrelated organisms.

    In light of this historical precedence, I interpret convergent features (analogies) as the handiwork of a Divine mind. The repeated origins of biological features equate to the repeated creations by an intelligent Agent who employs a common set of solutions to address a common set of problems facing unrelated organisms.

    Thus, the idea of monogamous convergence seems to divorce itself from the evolutionary framework, but it makes for a solid marriage in a creation model framework.

    Resources

    Endnotes
    1. Mark Binelli, “Gregg Allman: The Lost Brother,” Rolling Stone, no. 1082/1083 (July 9–23, 2009), https://www.rollingstone.com/music/music-features/gregg-allman-the-lost-brother-108623/.
    2. Binelli, “Gregg Allman: The Lost Brother.”
    3. Rebecca L. Young et al., “Conserved Transcriptomic Profiles underpin Monogamy across Vertebrates,” Proceedings of the National Academy of Sciences, USA 116, no. 4 (January 22, 2019): 1331–36, doi:10.1073/pnas.1813775116.
    4. Stephen Jay Gould, Wonderful Life: The Burgess Shale and the Nature of History (New York: W. W. Norton & Company, 1990).
    5. Simon Conway Morris, Life’s Solution: Inevitable Humans in a Lonely Universe (New York: Cambridge University Press, 2003); George McGhee, Convergent Evolution: Limited Forms Most Beautiful (Cambridge, MA: MIT Press, 2011).
    6. University of Texas at Austin, “Evolution Used Same Genetic Formula to Turn Animals Monogamous,” ScienceDaily (January 7, 2019), www.sciencedaily.com/releases/2019/01/1901071507.htm.

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