So far in this series, we’ve examined Casey Luskin’s attempt to cast doubt on human-chimpanzee common ancestry by (a) attempting to minimize the level of identity we observe when comparing our genome to the chimpanzee genome, and (b) claiming that the reason we see conservation of nearly all codons in humans and chimpanzees is because all of those codons encode a function beyond specifying an amino acid. As we have seen, those arguments do not hold up to scrutiny.
Luskin then turns to the evidence for common ancestry from shared synteny: the observation that humans and chimpanzees not only have nearly identical genome sequences, but that we have them in nearly identical spatial arrangements, across our entire genomes. Indeed, once again what we observe is exactly what one would predict for our two genomes to have if they had once been the same genome in our common ancestral population, with subtle modifications to this common structure occurring in our two lineages after they diverged. In the face of this evidence, once more Luskin is pressed to provide a non-evolutionary explanation for the pattern we observe – and, not surprisingly, he reaches for the same argument that he did for conservation of codons: functional constraint.
Function, function, everywhere (again)!
Luskin’s argument goes like this: spatial organization of genes on chromosomes is important for gene regulation; therefore the spatial organization of the human and chimpanzee genomes is under functional constraint; therefore a designer independently organized these two genomes for function in such a way that they are nearly identical in order to make them both functional – and the appearance of relatedness is entirely illusory. Put more simply, Luskin is arguing, once more, that the two genomes in question need to be nearly identical in order for them to work. In support of his argument Luskin quotes a number of recent papers describing work on functional organization of genomes, and claims that my science is “out of date.”
Unfortunately for Luskin, this argument also falls apart on closer inspection. For starters, none of the evidence he cites establishes that two genomes need to be (nearly) identical in order to work. The papers he cites are legitimate papers, and do provide evidence that genes on different chromosomes (or genes in different regions of the same chromosome) “find” and influence each other in important ways (for example, to regulate their transcription from DNA into RNA). While this is interesting, cutting-edge work, it simply does not follow that genomes are so tightly constrained in their spatial organization that (almost) all genes in two genomes need to be in the same places in order to perform their function. In fact we know, from multiple lines of evidence that Luskin fails to mention, that genomes are not constrained in this way.
The lines of evidence that refute Luskin’s claim are several. One such line of evidence (that I point out in the original paper that Luskin is critiquing, but with which he fails to engage) is that we see greatly divergent patterns of gene and chromosome organization in what are accepted, even among creationists, to be closely-related species. As aDrosophila (fruit fly) geneticist, I used the example of fruit fly genomes to illustrate this. Creationists generally accept that fruit flies are all members of the same “created kind” and that limited speciation within that “kind” has produced the various species we see today. All of these species, of course, have properly functioning genomes that work well for fruit fly biochemistry and cellular function. What is interesting for our purposes is that fruit flies have a very wide array of different synteny arrangements, a range that greatly exceeds the differences we see between humans and chimpanzees, in fact. If the designer was able to make fruit fly genomes that distinct, why was it not possible to achieve the same distinction between humans and chimpanzees? Humans and chimpanzees are more divergent in behavior and diet than fruit flies are, so if anything their genomes should be more distinct from each other if one were to appeal to a “common design” type argument.
Of mice and men
A second line of evidence comes from mammals, and extends the above observations to members of the same species. The humble house mouse, Mus musculus, has a dizzying array of synteny arrangements within one species. On the Portuguese island of Madeira alone, for example, there are six distinct “chromosomal races” of mice that have arisen from a common population introduced to the island by Europeans in the 1400s. The “standard” chromosome number for mice is 40, but on Madeira mouse populations with chromosome numbers ranging from 22 to 28 are found. These reductions in chromosome number are due to chromosome fusions, as you might expect. Beyond these changes, translocations have rearranged these fused chromosomes further in some populations. In other words, when examining Madeiran mice, we see huge differences in synteny that have arisen within the last 600 years. Again, this level of diversity within one species greatly exceeds the differences we see between humans and chimpanzees – and these mice, of course, all have perfectly functioning genomes that serve their needs just fine. From a “common design” perspective, one needs to explain why this level of diversity of genome organization can be designed for mice, but not for primates. Based on what we see in mice, we would expect a large number of highly divergent – yet equally functional – chromosome arrangements for any given mammalian species.
Last, but certainly not least, is the fact that humans themselves have a significant range of functional synteny arrangements as well. Chromosome translocations and fusions are also features we see in human genomes, and many of these alternate synteny arrangements are fully functional. One case from China that made the news in 2010 is a man with only 44 chromosomes instead of the standard 46: this man has not just one fused chromosome (chromosomes 14 and 15 are fused together in his case) but both his sets of 14 and 15 are fused. He inherited these fused sets from both his mother and father, who are distantly related – and the fused set ultimately comes from that distant relative, where the fusion occurred just once. As in most cases, this individual noticed no ill effects for themselves, but only fertility issues. When chromosomes with an “altered” arrangement attempt to match up with the “proper” set from the other parent, it may lead to embryos with a chromosome set that is unbalanced, with duplications and/or deletions of chromosomal material. The point, however, is that they themselves are fine, with no adverse effects. Moreover, if they were part of a population where everyone had their “alternate” arrangement, there would be no fertility issues at all – just like the populations of Madeiran mice, these hypothetical human populations would have “settled” on an alternative – but nonetheless perfectly functional – chromosome structure. As such, this shows that the human genome could easily be “designed” to be less similar to the chimpanzee genome than it is – after all, some of us do have genomes that are more distinct from chimpanzees than the “standard” human synteny arrangement, and there was nothing stopping a designer from making that the “standard” structure.
One section of Luskin’s attempted rebuttal of evidence for common ancestry from synteny actually makes this very point, but Luskin fails to see the irony. The largest difference in synteny between humans and chimpanzees is the chromosome fusion event that led to the modern-day human chromosome 2. The genetic material on this fused human chromosome is present on two shorter chromosomes in chimpanzees and other apes. Luskin’s main point here is that this fusion, which he accepts, was a human-only event: it happened once in the lineage leading to our own species, and eventually replaced the unfused chromosomes as the “standard” arrangement. (Presumably Luskin would then accept the Denisovan hominids as fully human, since they too have this fused chromosome, indicating that the fusion event occurred before Homo sapiens and the Denisovans diverged). The point here is this: Luskin accepts that a chromosome fusion event (meaning a large change in synteny) happened within the human lineage, with no ill effects. If indeed synteny was as tightly constrained as Luskin proposes, then this event should have had catastrophic consequences. The fact that this event led to the largest difference in synteny between humans and other apes only sharpens the point. For Luskin to remain consistent, he would have to argue that humans and chimpanzees were originally “designed” (i.e. created) with genomes even more identical than we see in the present day – which scuttles his argument that our genomes look the way they do because they had to be nearly identical. At a minimum, could not the designer originally have designed our two genomes to be at least as distinct as they are in the present day, but without any evidence for a fusion event? And if so, and the designer wished to avoid the impression of common ancestry to the full extent possible (despite the functional constraints Luskin supposes), why did the designer not do so?
Rather than engage in these sorts of highly ad hoc arguments against common ancestry, it is much more reasonable to conclude that what we see when comparing genomes arises from exactly what the evidence so strongly suggests: that God was pleased to create species, including ours, through an evolutionary process. The reason humans and chimpanzees have nearly identical synteny arrangements is because humans and chimpanzees once shared a genome in common, and only small changes to that genome’s structure have accumulated since our species diverged 4-6 million years ago.
In the next (and final) installment in this series, we’ll examine Luskin’s arguments about pseudogenes, and summarize how the all of the evidence we’ve examined coheres into a compelling pattern supporting human common ancestry.