Venema recently posted a second challenge to our model, focusing this time on the pseudogene evidence cited in favor of human evolution.
As I pointed out last week, when evolutionary biologists use the pseudogene argument, they make a number of assumptions: (1) pseudogenes must lack function; (2) their origin must be due to rare, random events; and (3) their juxtaposition to other genes must be arbitrary. Recent work questions the validity of these assumptions. But, as Venema points out in his critique, researchers have yet to discover function for unitary pseudogenes. He argues that this creates devastating problems for RTB’s human origins model. But is that the case? Can the RTB model make sense of shared junk DNA sequences that do not appear to have function?
I started addressing this question last week by presenting the framework for RTB’s genomics model. The RTB model can account for both the similarities and differences between organisms’ genomes in two ways: (1) as the deliberate work of a Creator; or (2) as the consequence of natural-process mechanisms that alter the genomes after creation.
This week, I would like to apply this model to the GLO pseudogenes found in humans and chimps. These unitary pseudogenes are often used to illustrate the argument for common descent and biological evolution.
The GLO Pseudogene and Vitamin C Synthesis
Most mammals make vitamin C (ascorbic acid) in their liver. But a few species have lost that ability due to a defect in the gene that encodes the protein responsible for directing the last step in converting glucose to ascorbic acid. This deficiency (referred to as the GLO pseudogene) plagues humans, chimpanzees and other primates, as well as bats and guinea pigs. These animals can survive, however, because they ingest enough vitamin C in their diet to make up for the lost ability to produce this key compound.
Humans and primates (including chimps) share many of the same mutations in the GLO pseudogene. Evolutionary biologists argue that these shared errors evince common descent and the shared ancestry of humans and the great apes. But if this defect arose before humans and chimp lineages diverged from a common ancestor, it would explain why both organisms share the same GLO pseudogene. Why would a Creator introduce exactly the same defective, nonfunctional DNA in both humans and chimpanzees?
The RTB Genomics Model and the GLO Pseudogene
Last week, I presented the basic tenets of the RTB genomics model, which includes the idea that similar genetic features reflect physical, chemical, or biochemical processes that occur frequently in a nonrandom, reproducible manner. This aspect of the model has the most relevance for explaining the shared features of the primate GLO pseudogene. In other words, the shared features of the GLO pseudogene arose independently, multiple times in humans and the great apes.
In rats, the GLO gene, which is functional, consists of 12 coding regions (exons). In humans the first six regions are missing, as is the next to the last one. Presumably these regions were lost due to some type of deletion event. Researchers have focused most of their attention on the tenth region (exon X), which consists of 164 base pairs (genetic letters).
Comparison of the rat’s exon X DNA sequence with those in humans, chimpanzees, and orangutans reveals a number of the same mutations in the same locations for the primate sequences. Of particular significance is position 97 in which it appears as if a deletion took place in the primate sequences. Evolutionary biologists argue that this deletion and the other shared mutations are clear evidence for common ancestry, with these changes having occurred before apes diverged from Old World monkeys.
The RTB genomics model offers a different explanation for the similarities in the primate DNA sequences. The shared features are interpreted as the outworking of nonrandom, reproducible changes that happened independently in humans, chimpanzees, and orangutans.
Support for this interpretation comes from comparisons of the primate exon X sequences with the corresponding region of the guinea pig GLO pseudogene. The structure of the guinea pig GLO pseudogene is dramatically different than that of the human pseudogene. Presumably, guinea pigs and primates lost this gene independently. If mutations were random, then few if any of the changes in the primate and guinea pig exon X sequences would be the same. Yet, as biologist Peter Borger points out, fifty percent of the mutations in the primate and guinea pig exon X sequence are identical. In addition, the guinea pig exon X region shows a mutation at position 97, the location in the primate genomes where a deletion took place. These shared features could not have resulted because guinea pigs and primates shared a common ancestor. Instead, they must reflect nonrandom, reproducible changes.
In other words, the RTB genomics model can reasonably account for the shared features of the GLO pseudogene in primates without resorting to common ancestry as the explanation.
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