As those who follow the American creation-evolution “wars” surely know, December 20th marks the 10 anniversary of the Kitzmiller vs. Dover decision (PDF). (For background on the Kitzmiller case, see here). This case garnered international publicity and ultimately ruled that teaching Intelligent Design (ID) was unconstitutional in the U.S. public school system. While I was still in my own ID wilderness myself, Ted Davis attended the trial in person and his article about the case remains an excellent read nearly a decade later. Ted has also written on ID in his excellent Science and the Bible series here on BioLogos.
Kitzmiller was a huge blow to the ID movement, and, not surprisingly, several of its leaders have expended significant effort to re-argue the case after the fact. The most recent of these attempts take the form of a series of posts at the Discovery Institute site Evolution News and Views entitled “10 Myths About Dover” – a series of posts intended to present the ID view at a time when many are recalling the events of a decade ago.
While the posts are fascinating for a number of reasons, it should come as no surprise that I am primarily interested in the biological details of the arguments on offer. In one post in the series, Casey Luskin asserts that one key line of evidence for common ancestry offered at the trial has now been shown to be incorrect:
On the opening day of the 2005 Dover trial, the plaintiffs' leadoff expert witness, noted anti-ID biologist Kenneth Miller, was asked, "Are you able to give us some examples of how modern genetics has applied to evolutionary theory?" His Exhibit A argument was to testify that the human beta-globin pseudogene is "broken" because "it has a series of molecular errors that render the gene non-functional." Since humans, chimpanzees, and gorillas share "matching mistakes" in the pseudogene, he told the court, this "leads us to just one conclusion ... that these three species share a common ancestor."
However, Miller's assertion, crucial to his testimony, is now known to be wrong. A 2013 study in Genome Biology and Evolution reported that the beta-globin pseudogene is functional.
Interestingly, this exact pseudogene has also been discussed by biochemist Michael Behe, a leading ID proponent. Like Miller, he too views it as compelling evidence for the common ancestry of humans and chimpanzees:
Chimp DNA has a very similar pseudogene at the same position. The beginning of the human pseudogene has two particular changes in two nucleotide letters that seem to deactivate the gene. The chimp pseudogene has the exact same changes. A bit further down in the human pseudogene is a deletion mutation, where one particular letter is missing. For technical reasons, the deletion irrevocably messes up the gene's coding. The very same letter is missing in the chimp gene. Toward the end of the human pseudogene another letter is missing. The chimp pseudogene is missing it, too.
The same mistakes in the same gene in the same positions of both human and chimp DNA. If a common ancestor first sustained the mutational mistakes and subsequently gave rise to those two modern species, that would very readily account for why both species have them now. It's hard to imagine how there could be stronger evidence for the common ancestry of chimps and humans.
Michael Behe, The Edge of Evolution, pp. 71-72
So, has new evidence overthrown a key anti-ID argument in Kitzmiller? If the case was re-tried today, would the case for common ancestry fail? Should Behe rescind his argument for common ancestry? Well, no – there is an abundance of evidence for common ancestry aside from the beta globin pseudogene example, even if we take Luskin’s argument at face value. All of that evidence does not suddenly evaporate even if the human and chimpanzee beta globin pseudogenes are found to have a function. That said, examining Luskin’s argument is an opportunity to learn more about the biology of pseudogenes, explore what “function” means, and discuss how antievolutionary groups represent pseudogene evidence to their constituents.
The human beta globin cluster
In order to understand the arguments Miller, Behe, and Luskin are making, we need to place the beta globin pseudogene in its biological context. Beta globins are a component of hemoglobin, the protein complex that is used to transport oxygen in the bloodstream. The hemoglobin protein complex is made up of four proteins: a pair of “alpha” globins and a pair of “beta” globins. In humans, the same alpha globins are used throughout development and adult life. There are five different beta globins, however, and they trade off at different stages in our development. We use one beta globin during embryonic development; two more during fetal development, and the remaining two after fetal development and on into adulthood. Despite using five different beta globin proteins, humans have six beta globin gene sequences clustered together on chromosome 11:
One of these globin sequences - beta globin “eta”, shown in blue - , is strikingly similar to a beta globin, but has sequence differences that indicate it cannot function as a beta globin protein – the differences are such that this sequence cannot be translated into a protein by the cell. It is these differences that Miller and Behe are referring to in their arguments, since these differences are also found in chimpanzees as well as humans.
The standard evolutionary explanation for these observations is straightforward: the beta globin pseudogene arose as a duplicated gene (as did all of the six at one point or another, actually) but was rendered non-functional due to mutations. The fact that we observe the same pseudogene in the same location with the same mutations in chimpanzees indicates that the duplication event and subsequent mutations inactivating the gene occurred prior to the common ancestral population of humans and chimpanzees separating some 4-6 million years ago. To argue otherwise is to argue that both species arrived at their present states independently of each other – an argument that neither Miller nor Behe find plausible.
Yet it is this argument that Luskin appears to support, based on a recent study that shows that the beta globin pseudogene may indeed have a function:
Ken Miller's argument for Darwinian evolution, and against ID, depends on the beta-globin pseudogene being "non-functional," implying as he does that the genetic differences between it and protein-coding beta-globin genes are errors. In light of this new evidence for the functionality of the beta-globin pseudogene, it seems that those genetic differences may not be errors at all. If so, then Miller's argument, his Exhibit A, collapses.
In tomorrow's post, we’ll explore that evidence, consider its implications for ID, and use it to evaluate Luskin’s case that Miller’s argument from Kitzmiller is no longer valid.