In case you haven't run into it, there's been a bit of a kerfuffle about theistic evolutionist Karl Giberson's use in a debate of a photoshopped image of a human baby with a tail. Eventually, with a monumentally bad grace combined with silly comments on his public Facebook page about Homer Simpson, Giberson apologized for accidentally using a photoshopped image. We can therefore assume he won't keep using it in debates.
Thus ends Tailgate, at least as regards the image aspect thereof. In the course of following all of this, though, I became rather interested in the claims being made about allegedly atavistic human tails which are, Giberson still insists, evidence for common descent between humans and tailed ancestors.
Here are a couple of things Giberson says on this subject. (Some of these are from a long thread on Nancy Pearcey's set-public Facebook wall.)
Here he says,
I asked the challenging question: “Why does the human genome contain instructions for the production of features we don’t use?” The scientific explanation is that we inherited these instructions from our tailed ancestors but the instructions for producing them have been shut off in our genomes, which is why Shallow Hal is the only person most people know who has a tail. Sometimes the “ignore these genes” message gets lost in fetal development, however, and babies are born with perfectly formed, even functional tails.
On the public Facebook thread he says,
In the discussion I also reference an article identifying the actual human gene for tails (same as the mouse gene, except ours is shut down.) If, for example, I accidentally showed a photo of Plato when talking about Aristotle that would be an irrelevant error. At no point did I imply that the image I showed was evidence. It was illustration.
He also claims that this is "bad design,"
The "common ancestry" and "bad design" evidences go together. It is bad design for our genomes to have dormant DNA that may or may not kick in. Common ancestry explains why.
And metaphorically speaking, shakes his head,
I have no idea how Intelligent Design theorists explain humans with tails.
Well, I'd like to help out. Here, not from Karl Giberson, is a scientific hypothesis about the reason why some human babies are born with tails:
As discussed below in detail, the development of the normal human tail in the early embryo has been investigated extensively, and apoptosis (programmed cell death) plays a significant role in removing the tail of a human embryo after it has formed. It is now known that down-regulation of the Wnt-3a gene induces apoptosis of tail cells during mouse development (Greco et al. 1996; Shum et al. 1999; Takada et al. 1994), and similar effects are observed in humans (Chan et al. 2002). Additionally, researchers have identified a mutant mouse that does not develop a tail, and this phenotype is due to a regulatory mutation that decreases the Wnt-3a gene dosage (Greco et al. 1996; Gruneberg and Wickramaratne 1974; Heston 1951)....[A] mutation or environmental factor that increased dosage of the Wnt-3a gene would reduce apoptosis of the human tail during development and would result in its retention...in a newborn.
Now, there's a big reveal coming up here in a minute, folks, and it's related to the ellipses in that quote and to the fact that I didn't give the link for that quote, so bear with me, here. Nothing will be hidden in the end, but I'd like to tell this in a particular order.
First, what is this WNT-3a gene? From Giberson's description, one would think that it is a "gene for tails" and that it is normally "switched off" in human beings. But if one thought that, one would be wrong on both points. As five minutes' googling reveals, this is the WNT-3a gene. It is not a gene for tails per se, and it is not switched off in humans. Rather, it is an important regulatory gene that, in humans, serves a function "in cell-cell signaling during morphogenesis of the developing neural tube." The neural tube, in case you were wondering, is the embryonic precursor to the central nervous system, including the brain and the spinal chord. Rather an important human gene, that.
The theory given in the above quotation is that some random, individual event in the conception of a particular human embryo results in a higher gene dosage of the WNT-3a gene. Not, mind you, in its being switched on when it was previously switched off. It fulfills an important function in human development, so it isn't switched off at all. Gene dosage, we learn, is "the number of copies of a given gene present in the cell of an organism." So the theory is that some babies are conceived by happenstance with a higher number of copies of the WNT-3a gene in their cells.
Normal human embryos go through a transient stage in which the spinal chord extends longer than it will ultimately need to be. This is the famous "tail." This extra-long portion of the spinal chord then normally regresses as part of the process of human development in utero. The theory is that a higher gene dosage of the (important and functional) WNT-3a gene causes a failure of this disappearing mechanism, resulting in a human baby born with a tail-like structure.
So let's help out Karl Giberson, who cannot imagine how ID theorists explain human babies with tails. Here goes: Humans are designed with the very important and functional WNT-3a gene. This is not bad design but good design. This regulatory gene serves an important function in human development of stuff like the brain and spine--stuff we really need. This important and functional gene isn't leftover flotsam from some time millions ago in evolutionary history. Rather, it was designed for a purpose and actually works for that purpose in human beings. That the same regulatory switch also appears to be involved in the development of tails in other creatures is irrelevant, since a designer can use the same switch for different downstream outcomes in different things he designs, and indeed WNT-3a apparently is serving partially different functions in humans and in other creatures. Occasionally an embryo is conceived, by the pure contingencies of biology which we have no reason to believe have anything whatsoever to do with tailed ancestors, with a defect, like any other birth defect. The nature of this defect is that the child has too much of a good thing--too many copies in his cells of this otherwise important and useful WNT-3a gene. This unnecessarily high gene dosage causes a failure of the normal disappearance of the extra portion of the baby's spinal chord in utero. As Casey Luskin points out here, it also usually causes other problems in the child, as one would expect given that human beings were not designed to have tails (or that many copies of WNT-3a).
Now, that's just a theory. It may be that a high gene dosage of WNT-3a is not responsible for the fact that some babies are born with tail-like structures. However, it appears to be the only theory currently connecting what Karl Giberson calls "the gene for tails" (namely, WNT-3a) with babies born with tails. In other words, it's the only visible candidate for the theory about a gene that Karl Giberson is alluding to. The problem is that this theory about this gene is completely different from what Giberson said. It does not require us to describe WNT-3a inaccurately as "a gene for tails." A moment's research shows that it is actually a gene involved in a variety of things, including neural tube development in humans. The theory, contra Giberson, isn't that the gene is switched off (which it isn't). And the theory, contra Giberson, isn't that this gene is non-functional junk that causes babies to be born with tails when the gene accidentally gets switched on or is accidentally "not ignored." In other words, Giberson is just incorrectly describing the whole theory about how WNT-3a is involved in the birth of human babies with tail-like structures. (See also Casey Luskin's discussion of the "switched-off gene" claim here.)
Now comes the big revelation. I just quoted the theory that Giberson is inaccurately explaining concerning WNT-3a from the pro-evolution web site TalkOrigins, where they nonetheless think that the fact that babies are sometimes born with tails is evidence for common ancestry. In fact, one theistic evolutionist and one person highly sympathetic to that view sent me the TalkOrigins link as though it supported Giberson's position rather than contradicting it! Here is the link, and here is the quotation with a little lead-in and without the ellipses:
As with other atavistic structures, human tails are most likely the result of either a somatic mutation, a germline mutation, or an environmental influence that reactivates an underlying developmental pathway which has been retained, if only partially, in the human genome (Dao and Netsky 1984; Hall 1984; Hall 1995). In fact, the genes that control the development of tails in mice and other vertebrates have been identified (the Wnt-3a and Cdx1 genes; Greco et al. 1996; Prinos et al. 2001; Schubert et al. 2001; Shum et al. 1999; Takada et al. 1994). As predicted by common descent from the atavistic evidence, these tail genes have also been discovered in the human genome (Katoh 2002; Roelink et al. 1993). As discussed below in detail, the development of the normal human tail in the early embryo has been investigated extensively, and apoptosis (programmed cell death) plays a significant role in removing the tail of a human embryo after it has formed. It is now known that down-regulation of the Wnt-3a gene induces apoptosis of tail cells during mouse development (Greco et al. 1996; Shum et al. 1999; Takada et al. 1994), and similar effects are observed in humans (Chan et al. 2002). Additionally, researchers have identified a mutant mouse that does not develop a tail, and this phenotype is due to a regulatory mutation that decreases the Wnt-3a gene dosage (Greco et al. 1996; Gruneberg and Wickramaratne 1974; Heston 1951). Thus, current evidence indicates that the genetic cause of tail loss in the evolution of apes was likely a simple regulatory mutation(s) that slightly decreased Wnt-3a gene dosage. Conversely, a mutation or environmental factor that increased dosage of the Wnt-3a gene would reduce apoptosis of the human tail during development and would result in its retention, as an atavism, in a newborn.
Notice several things about this. First, the lead-in sentence, taken in conjunction with what the theory actually is in the rest of the paragraph, gives us a garbled picture. The lead-in sentence implies that a "developmental pathway" in humans for tails is somehow inactive and needs to be "reactivated." Giberson has tried to spell this out by saying that there is a "gene for tails" that is "switched off" and has to be "switched on," which as we have seen is false. But the lead-in sentence, though less explicit than Giberson and hence less subject to outright falsification, is also in tension with the rest of the paragraph. What is this "inactivated developmental pathway," precisely, if the actual mechanism of human babies' birth with tails is an excessive cellular dosage of a needed and functional human gene? It seems quite misleading to call such an accidental excessive dosage (and the description itself makes the accidental nature in the individual quite clear) a "reactivation" of anything whatsoever, unless of course one is already committed to the proposition of common ancestry. But on that construal, the argument from babies born with tails to common ancestry is circular.
Similarly, the passage refers to "these tail genes" as being discovered in humans, and refers to this as "predicted by common descent." Perhaps this is where Karl Giberson got his ideas. But as one reads on, one learns that the gene in question is WNT-3a, which, one can discover by a small amount of research, is not per se a tail gene and is not deactivated in humans but is rather a functional gene in humans.
The reference to the "genetic cause of tail loss in the evolution of apes" is pure speculation based upon the assumption of common ancestry. There is nothing in the hypothesized cause of occasional human tail-like structures (extra-high gene dosage of WNT-3a) that supports this as a conclusion as over against common design using WNT-3a for the variety of functions that we know it presently has. Similarly, the use of the terms "atavistic" and "atavism" play no explanatory role as regards why a particular baby's extra spinal chord segment does not regress in utero. The passage already conjectures that this is caused by a chance mutation in recent time or even an environmental cause--in other words, by a random event connected to that embryo that is not caused by the past evolutionary history of humans as the authors conjecture it.
So what we have here is an actual scientific hypothesis concerning how particular human babies might come to be born with tail-like structures, but it is mingled with random references to conjectural evolutionary claims that are doing no explanatory work. This mingling produces a weird hodge-podge that the unwary might take to mean that WNT-3a has no function in humans and is just leftover flotsam and jetsam. Even a short googling turns up the falsehood of that claim, which the TalkOrigins author doesn't explicitly make in any event. Karl Giberson fleshes all of this out into far more explicit, but flatly wrong, claims that we humans have a leftover "gene for tails" from our species' evolutionary past that would be "bad design" if it were designed and that is "switched off" or "ignored" in human development and occasionally gets accidentally "switched on," causing babies to be born with atavistic tails!
If we strip away all the misleading talk about "reactivation" and the outright falsehood that the relevant gene is a leftover piece of junk that is switched off in humans, what is left of the argument for common descent from the fact that human babies' extra spinal chord section sometimes doesn't regress before birth? Precious little. In fact, almost nothing but the morphological resemblance of the resultant structure to a tail. As in, "Hey, look, a human baby with a tail! Gee, I wonder if that means we were descended from an ancestor with a tail! Because, see, it's a tail!" By itself, this is an exceedingly weak argument, to put it charitably. What if an occasional human baby were born with a third arm? Let us say, even, that it were a functional arm that could be moved. Would that give us any reason at all to believe that we were descended from ancestors with three arms? The negative answer should be evident. Weird, abnormal glitches happen in embryonic development all the time. Thalidomide babies are born with no arms, but that doesn't mean we were descended from ancestors with flipper-like hands attached directly to their shoulders.
I suppose one might add, to try to wring as much as possible out of the remaining data, that we do not know why humans go through a transient phase in utero in which their spinal chords are extra-long and then regress. But talk about "Darwinism of the gaps"! "We don't know why this happens, so maybe it has something or other to do with evolutionary history!" Considering that we do know that the WNT-3a gene is functional and important in neural tube development, it would be the height of folly to assume that having less of it would be a good thing on the grounds that (maybe) down-regulation of WNT-3a would result in a shorter human spinal column in utero all along rather than the normal, transient "tail" development phase. This point fits well with the fact that evolutionary reasoning has already been medically harmful, as Casey Luskin points out: Assuming that babies born with tail-like structures have merely a harmless atavism and are otherwise perfectly healthy has led to a failure to look for other medical problems, which usually do turn out to be present.
The cautionary tale here is not hard to find: When an evolutionary theorist, even a theistic evolutionist, tells you as an assured fact that some human structure is caused as an atavism by a leftover and normally switched-off gene from our evolutionary past, don't be in too much of a hurry to believe him. In this case, it turns out that Giberson's characterization is wrong even by comparison with what his fellow evolutionists are saying. As for his rush to infer "bad design," what is one to say? When the gene in question is, in fact, working just fine, thanks very much, in human neural tube development, the characterization of its existence as "bad design" cannot stand up for a moment. But of course that characterization is of a piece with the inaccurate claim that the gene is normally "switched off" and "ignored."
I am not claiming that there are no segments of the human genome that do not have presently known functions. These are the segments that scientists have recklessly been calling "junk DNA" for quite a while, though a variety of recent developments may be teaching them a little more humility and caution. I'm not even claiming to know for sure that there is no actual, non-functioning junk in the human genome, were all known. In this case, however, the gene in question is not even alleged by mainstream science to be non-functional. It would be the sheerest conjecture to try to figure out where Karl Giberson got that idea. For the rest of us, I would just say: Checking these things out for yourself often pays off handsomely.