Gene Splicing May Account for the Biological and Behavioral Distinctions of Humans
Chimpanzee exhibits top many people’s list of favorite zoo attractions. Watching these apes carry on delights human observers of all ages. The antics of chimps, often compared to human behavior, are not the only thing about these wonderful creatures that captivates the interest of humans. Genetic comparisons between chimps and humans generate their fair share of fascination.
The high degree of genetic similarity between humans and chimpanzees represents one of the most popular and seemingly convincing arguments for the evolutionary origin of man. Presumably, the 95-99% overlap of DNA sequences indicates that humans and chimpanzees arose from a common ancestor in the relatively recent past (about 6 million years ago).
Yet a number of other studies suggest that humans and chimpanzees may be much more genetically distinct than commonly believed. And these differences appear to show far more biological and behavioral significance than the overlap in DNA sequences. (See here and here for recent discussion on some of these genetic differences.)
DNA is the molecule that harbors genetic information within a cell. This information essentially consists of the instructions necessary to make and regulate the activity of all the proteins used by the cell. The region of the DNA molecule that specifies the production of a single protein chain is called a gene.
Proteins, the “workhorse” molecules of life, take part in virtually every cellular and extracellular structure and activity.
Protein production begins when the cell’s machinery makes a copy of the information housed in a gene by assembling a molecule known as messenger RNA. Once assembled, messenger RNA migrates from the nucleus of the cell into the cytoplasm. At the ribosome, messenger RNA directs the synthesis of the protein.
In humans and chimps, after messenger RNA is produced, it undergoes extensive modification before it heads to the ribosome. The final modifications to messenger RNA involve the so-called splicing reactions. In eukaryotes, the sequences that make up a gene consist of stretches that code for part of the protein (called exons) interrupted by sequences that don’t code for anything (called introns). After the gene is copied by assembling the messenger RNA, the intron sequences are excised from the messenger RNA and the exons spliced together. A RNA-protein complex called a spliceosome mediates this process.
Remarkably, the spliceosome can splice a single messenger RNA in different ways to produce a range of functional proteins. Known as alternate splicing, this variation is possible because the spliceosome does not necessarily use all the splice sites. Structuring genes to contain non-coding regions (introns) interspersed between coding regions (exons) serves as an elegant strategy that allows a single gene to simultaneously house the information to produce a range of proteins.
Chimps and Humans Differ in Alternate Splicing
For the first time, researchers have examined differences in alternate splicing between humans and chimpanzees. Even though no one had previously compared alternate splicing in humans and chimpanzees, researchers hoped to see differences, since about two-thirds of genes in humans and mice undergo alternate splicing and complex alternate splicing reactions are unique to tissues and organs.
The researchers discovered that a significant proportion of alternate splicing reactions in humans, chimps, and mice are highly similar. From an evolutionary perspective, this means that the splicing reactions haven’t evolved over the span of 80-90 million years. This makes sense. Splicing is an extremely precise process. Mistakes in splicing are responsible for some human diseases. Medical disorders, such as atherosclerosis, cardiomyopathy, and myotonic dystrophy, result because splicing errors fatally distort or destroy the information—temporarily stored in messenger RNA—needed to assemble protein chains at ribosomes. And improperly produced proteins cannot carry out their functional role in the cell.
In spite of what appears to be the resistance of alternate splicing patterns to evolve, the researchers also noted that six to eight percent of the genes examined in their study displayed differences in alternate splicing patterns in humans and chimps. And it appears that these differences evolved rapidly. The alternate splicing differences were observed for both brain and heart tissues and involve genes that take part in diverse functions. These results suggest that differences in alternate splicing patterns could account for some of the biological and behavioral differences between humans and chimps.
More and more, it appears that humans and chimps display key genetic differences where it counts. And these differences explain why humans visit the chimpanzee exhibit at the zoo, and not the other way around. For more information on these kinds of genetic comparisons between humans and chimps and how they fit into a biblical framework see an article I wrote for a recent issue of Connections or the book Who Was Adam?