We continue our review of the book, Adam and the Genome: Reading Scripture after Genetic Science, by Dennis Venema and Scot McKnight. Today, Chapter 2- Part 2
Chapter 2 begins with a brilliant analogy of how evolution works by comparing how Modern English evolved from ancient Anglo-Saxon. The major points of the analogy were:
- The various examples from the fossil record are not instantaneous changes from one to the next.
- They are samples drawn at intervals from a continuous process.
- Over time, however, changes accumulated that gradually shifted the average characteristics of the language / population as a whole.
- Given enough time, it becomes more and more of a stretch to say the language or the organisms are the same.
- Despite the striking differences we see now, the process that produced them was gradual.
- There is no convenient point where we can say Anglo-Saxon “became” Modern English or apes “became” humans; the process was a continuum.”
Dennis then talked about how DNA is composed of 4 “letters” and how those “letters” are used to replicate and code for proteins that do the “heavy lifting” work of the cells/organism, and how redundancy was built into that process. He then gave the example of the insulin protein and how knowing how DNA sequences code for that protein allows us to compare one organism’s sequence to another, in the first case dog to human. Then in his second example, comparing human, apes, and dog insulin. Based on anatomical characteristics, evolutionary theory predicts that these ape species share a more recent common ancestral population with humans than non-primate species such as dogs, do. If that is so, then their gene sequences should be a closer match to human sequences than what we observe in dogs. And that is, in fact, what we observe, and this level of identity far exceeds what is needed for functional insulin. We have failed to reject the hypothesis that humans share a common ancestral population with apes.
The pattern that was observed in the insulin gene sequence has now been confirmed to exist across numerous other gene sequences of humans and great apes. Beyond genes, our entire genomes are either around 95% or around 98% identical, depending on how one counts the effect of deletions of small blocks of DNA. And not only nearly identical, but organized in the same spatial pattern. In the book analogy, at the sentence, paragraph, and chapter level, our two “books” are organized in the same way.
The next example Dennis gives for shared ancestry are the olfactory receptor genes, or simply put, our sense of smell. Mammals on the average have about 1,000 genes devoted to the sense of smell, out of a total gene count of 25,000; which means a significant proportion dedicated to this purpose. Mammals that hunt (like wolves) have very keen senses of smell because their olfactory genes are kept in good repair—deleterious mutations are weeded out through selection. Humans have a diminished capacity for smell; and the reason became apparent after the human genome was sequenced. Many of our olfactory receptor genes are damaged (mutated) but they persist because the mutations are replicated once they are “locked” in. As a result these genes persist as genetic “fossils” in our DNA. They are known as “pseudogenes” (false genes) because they have many of the features of genes but cannot translate as a gene should to produce a useful protein product. Now, not only do other primates have mutations in their olfactory receptor genes, but the same genes are lost and often the exact same mutation event, down to the exact DNA letter change, is seen in more than one species.
So in the first example from Figure 2-7, the gene 5AK4p is shared among all 4 species. It has a “stop” mutation at DNA letter 236, which is a mutation that “stops” the gene from coding for the amino acids necessary to do its job. So what is the reason all 4 species share the same mutation? It could be coincidence that the same mutation occurred 4 times independently in different species. A second possibility is that the mutation occurred once in a common ancestral population to all 4 species, and subsequently inherited by all 4 species. The paper Dennis is citing also observes that several mutated genes fit this pattern. Even if one gene might have this pattern by chance, it is extremely unlikely that numerous genes would have this same pattern by change alone. Heredity is the more parsimonious explanation and, again, we have failed to reject the hypothesis that humans share a common ancestral population with apes.
A second pattern we observe is shown by gene 2; in this case, a deletion mutation (i.e. one DNA letter missing) at position 212 in humans, chimps, and gorillas, but not orangutans. Deletions mess up the code so that the mutated codon will code for the wrong amino acid—that ruins the protein’s function. Again, the simplest explanation is that this mutation occurred once in the population ancestral to humans, chimps, and gorillas and that the ancestral lineage for orangutans had already separated by this time. Once again the researchers found many examples that fit this pattern.
A third pattern in gene 3 shows a mutation shared only by humans and chimps. Again, the simplest explanation is that this mutation occurred once in the population ancestral to humans and chimps, and that the ancestral lineage for orangutans and gorillas had already separated by this time.
Finally, we see mutations unique to a single species (genes 4-7). Such mutations are expected, since each species also has a period of unique history after its lineage separates from all the others.
Note, however, what we DON’T see: mutations shared by gorillas and chimps, but not seen in the other species, for example; or mutations shared by humans and orangutans that are not also seen in gorillas and chimps.
Why don’t we see these categories? Because the species are related in the manner suggested by the patterns we do see, therefore, we would not expect them. The data form a pattern called a “nested hierarchy”, which is a fancy name for a family tree. While this was worked out on the basis of partial genome sequencing, we now have full genome sequencing for all 4 species, and the genome-wide identity between humans and other apes follows the same pattern. Again, we have failed to reject the hypothesis that humans share a common ancestral population with apes.
Now the astute observer might ask; if this is true for humans and primates, then it must also be true if whales descended from land-based artiodactyls. Dennis answers that:
“In fact, DNA evidence comparing a modern artiodactyl (hippos) and modern cetaceans was the first evidence that these species share a common ancestral population, before the key diagnostic fossilized ankle bones were found in ancient whales. Not surprisingly, paleontologists doubted the new DNA science until they found the fossils that confirmed its predictions. DNA and fossils tell the same story; they are converging lines of evidence.”
Dennis then discusses the case of vitellogenin pseudogenes in placental mammals. (Note: I am borrowing language from Dennis’ articles at Biologos to save me time hand typing from the book. Dennis’ discussion in this book is a condensed version of the 5 articles he posted at Biologos on the Vitellogenin issue. See http://biologos.org/blogs/dennis-venema-letters-to-the-duchess/vitellogenin-and-common-ancestry-understanding-synteny.) Vitellogenins are large proteins used by egg-laying organisms to provide a store of nutrition to their embryos in egg yolk. Evolution would predict that all placental mammals once had vitellogenin genes in their genome, even if those genes would no longer be useful, if they did indeed shared a common ancestor in the past.
Modern birds (such as chickens) have three vitellogenin genes: VIT1, VIT2, and VIT3. The latter ones sit side by side in the chicken genome, with VIT1 in a different location. The three VIT genes sit next to other genes in the chicken genome: VIT1 sits next to a gene called “ELTD1”, and VIT2 and VIT3 sit between genes named “SSX2IP” and “CTBS”. These genes are not involved in making egg yolk – they just happen to be the closest neighbors of the VIT genes. With these data in hand, the researchers then searched the human genome for the genes near to the chicken VIT genes. These three genes (ELTD1, SSX2IP, and CTBS) are also found as functional genes in humans – and as expected, these genes have the same spatial arrangement in the human genome as they do in chickens.
Figure 2-9: The VIT1 and VIT2, VIT3 regions in the chicken and human genomes. White boxes indicate functional genes. Black boxes indicate sequence matches between the two genomes. The ELTD1, SSX2IP, and CTBS genes in humans and chickens are highly similar and line up with one another when comparing these regions. Small fragments of matching sequence can be seen covering both regions, including fragments matching portions of the chicken VIT1, VIT2, and VIT3 genes, though the most extensive matching is see in the fragmentary human VIT1 pseudogene.
To put it simply: we have a gene (no longer working) for making egg yolk. Why? WHY would God create us de novo with a gene for making egg yolk in our DNA? It makes perfect sense if God created us through a natural biologic process of descent with modification.
Dennis notes that given the abundant lines of DNA evidence that support the hypothesis that humans are the result of a natural biologic process, it is no exaggeration to say that very, very, few trained biologists reject common ancestry for any other reason than prior religious conviction. Dennis is friends with Todd Wood, who holds to a young earth creation position, but is one of the very few YECs who will engage the science honestly. Dennis quotes from an article on Todd’s blog from 2009:
Evolution is not a theory in crisis. It is not teetering on the verge of collapse. It has not failed as a scientific explanation. There is evidence for evolution, gobs and gobs of it. It is not just speculation or a faith choice or an assumption or a religion. It is a productive framework for lots of biological research, and it has amazing explanatory power. There is no conspiracy to hide the truth about the failure of evolution. There has really been no failure of evolution as a scientific theory. It works, and it works well.
I say these things not because I’m crazy or because I’ve “converted” to evolution. I say these things because they are true. I’m motivated this morning by reading yet another clueless, well-meaning person pompously declaring that evolution is a failure. People who say that are either unacquainted with the inner workings of science or unacquainted with the evidence for evolution. (Technically, they could also be deluded or lying, but that seems rather uncharitable to say. Oops.)
Creationist students, listen to me very carefully: There is evidence for evolution, and evolution is an extremely successful scientific theory. That doesn’t make it ultimately true, and it doesn’t mean that there could not possibly be viable alternatives. It is my own faith choice to reject evolution, because I believe the Bible reveals true information about the history of the earth that is fundamentally incompatible with evolution. I am motivated to understand God’s creation from what I believe to be a biblical, creationist perspective. Evolution itself is not flawed or without evidence. Please don’t be duped into thinking that somehow evolution itself is a failure. Please don’t idolize your own ability to reason. Faith is enough. If God said it, that should settle it. Maybe that’s not enough for your scoffing professor or your non-Christian friends, but it should be enough for you.
Todd took a lot of grief from the YEC community which goes to show their disingenuous attitude. I don’t how else to say it. He wasn’t being a “closet evolutionist” as he was called, he was being honest about the state of the evidence. It reminds me of the Glenn Morton story .
The thing is that Darwin nor any of his contemporaries, except maybe Gregor Mendel, could have imagined that organisms would retain a text-like record of their evolutionary past in their hereditary material. Genetics and the DNA evidence could have overturned the whole evolution theory. Genome sequencing could have rejected the hypothesis of common ancestry. In actuality, these new technologies have provided some of the most detailed and convincing evidence of descent with modification i.e. EVOLUTION.
Humans do share common ancestors with other apes; apes share common ancestors with other mammals; mammals share ancestors with other tetrapod vertebrates; tetrapod vertebrates, as we have seen, share ancestors wit fish; and ultimately all life on earth shares common ancestors dating back over 3 billion years.