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A Cautionary Tail

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.

Comments (19)

Both evolutionary design and intelligent design are like each other in that they are essentially design algorithms. A picture graces the cover of Time Magazine, people are amazed at it. The photographer wins Pulitzers, becomes a celebrity in his own right. How did he do it? Well the ID method might be that he carefully thought about where a really photogenic event would take place. He carefully selected his spot and equipment and with a tiny bit of luck snapped it. An evolutionary method might be he takes thousands upon thousands of pictures. When he gets back from his trip he puts them all up on his giant monitor and quickly pages through noting the promising ones, then he takes the hundreds of promising ones repeating until he narrows them down to one that is the best. If he does this every week for his entire career some of those best pictures are going to be really, really good.

Problem here is I don't think you can just look at the finished product and say which method was used. This is a problem for evolutionists trying to argue against ID. As you note there's nothing preventing a designer from reusing 'switches', even letting 'junk' and useless DNA creep into the code. But this is a fatal problem for ID theory.

ID theory is premised on looking at certain designs and asserting that they could only have been made 'intelligently'. No mechanism for making this determination has ever been presented by ID advocates. The closest they ever came is the irreducible complexity, which means something that could not be derived from the evolutionary steps of random mutations that are then selected for fitness. But no method of calculating this has ever been proposed, the best they have is to just look at something and shrug and say "I don't see how evolution could have made that". Well to make these statements you need to calculate every possible thing that evolution could make and show how that thing is not in that set. This would be more difficult than calculating the set of all possible chess games (which, last I read, would require a computer larger than the universe itself).

But no method of calculating this has ever been proposed, the best they have is to just look at something and shrug and say "I don't see how evolution could have made that".

This makes one wonder how much ID material you have actually read.

Moreover, the argument is not merely eliminative but is comparative and explanatory. We know the kinds of things that intelligent agents make. We know approximately what real teleological intention looks like. Living things have those types of properties. Comparatively speaking, the probability is _far lower_ given evolutionary mechanisms. It is not necessary absolutely to _rule out_ a non-design mechanism to make a comparative probabilistic argument.

In any event, this post is, specifically, about the argument _for_ common ancestry _from_ allegedly atavistic tails. I think that I have quite sufficiently shown that argument to be poor. Remember that the neo-Darwinist claims that his position has overwhelming evidence in favor of it. Multiple sources claim that these kinds of "atavistic traits" are part of this allegedly overwhelming evidence. It is therefore relevant to show one of those arguments to be poor.

Gilberson tipped his hand in some comments he recently made on Facebook:


Karl Giberson I refer to the study by Larson and Witham, considered definitive. Also some more recent work by Elaine Ecklund. Miracles are more complicated and less relevant. Loads of Christians reject virtually all miracles save the resurrection and even define that in a different way.
June 11 at 6:03pm · Like

Robert Firestone At what point is the word "Christian" even meaningful without the bodily resurrection?
June 11 at 6:05pm · Like · 1

Karl Giberson You should read Hans Kung or other leading theologians who explain that. I am not a theologian. I was once, rather provocatively, asked to "draw the trajectory of the ascension." Try it....
June 11 at 6:12pm · Like

https://www.facebook.com/paul.k.moser/posts/10152175853098947

If we take Boonton's alternate scenarios seriously, the first seems the much more likely explanation. The second is going to result in a photographer whose Pulitzers will come at far remove from each other, if at all, let alone allow him to make a living.

ID theory is premised on looking at certain designs and asserting that they could only have been made 'intelligently'. No mechanism for making this determination has ever been presented by ID advocates.

I'm probably out of my depth, but what does "mechanism" actually mean here? If I look at a chair and conclude that a man designed it, what is the answer to the question: by what mechanism was this determination made? See my problem?

Irreducible complexity, btw, is not a mechanism.

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.

Unless it is a pseudogene, no credible biologist would arrive at the inference that it has no function at all, given that it (presumably) evolutionarily conserved as purifying selection would remove any dysfunctional polymorphisms that would arise through mutation.

Rather, it was designed for a purpose and actually works for that purpose in human beings...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.

Why would an IDist say that it was designed for a particular purpose in humans? A gene that served a particular function in on particular species can have an orthologue that serves a different function in a different organism with a different ecological niche and development trajectory. Leaving aside the misconception that a gene can code "for" a morphological trait (of course many genes are named after the altered phenotypes of the mutants and Wnt (wingless) is an example), Wnt-3a has numerous homologues through the animal kingdom, and was certainly present in the first tetrapods (such as Tiktaalik and Icthyostega) that would be the common ancestor of all extant mammals, reptiles, amphibians, and birds (aside from that, it was originally discovered in the model organism Drosophila). The fact that Homo sapiens also possess a functional copy of Wnt-3a, whatever its precise developmental role is, as opposed to the gene totally being expunged from the human genome, suggests that the human lineage reflects an evolutionary connection with all of the ancestors of the ancient tetrapods and more generally all of the kingdom Metazoa.

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.

Actually, Larry Moran's blog covers the ENCODE "death of junk DNA hype"; most of the genome is practically non-functional

(Latias, I deleted a duplicate of your comment, FYI.)

Why would an IDist say that it was designed for a particular purpose in humans?

My point is simply that if WNT-3a is doing a good job at serving an important function in humans, then, if you think humans were designed, you will probably think it was designed to serve that function. Nothing heavier than that.

The fact that Homo sapiens also possess a functional copy of Wnt-3a, whatever its precise developmental role is, as opposed to the gene totally being expunged from the human genome, suggests that the human lineage reflects an evolutionary connection with all of the ancestors of the ancient tetrapods and more generally all of the kingdom Metazoa.

It doesn't suggest that to me. Why should it? Unless one assumes that similarity of functional genes always indicates common ancestry. And that's what we're arguing about, isn't it? The alternative to common descent isn't chance. Common design is also an alternative. The fact that your toaster and your microwave oven both have wires inside doesn't "suggest" that they were descended by non-designed processes from a common ancestor with wires.

As for the junk DNA meme, ENCODE is only part of the case against it, as pointed out here.

http://www.evolutionnews.org/2012/09/why_the_case_fo_1064771.html

It's not as though Moran is the last word on the subject, either. Jonathan McLatchie points out that Moran's own predictions about transcription have already been falsified, so he's just backing up:

http://www.evolutionnews.org/2012/09/perspectives_on064741.html

http://www.evolutionnews.org/2012/09/why_all_the_fus_1064721.html

It is _incredibly_ unscientific to call DNA of unknown function "junk." Talk about a science stopper. And to double down and be dogmatic about it is worse still.

Steve Hays, thanks for that info. Nothing like "defining the resurrection differently," is there?

Casey Luskin on Larry Moran's hysterical and politicized response to ENCODE:

http://www.evolutionnews.org/2012/09/what_an_evoluti_1064101.html

Jonathan McLatchie on giving science time:

http://www.evolutionnews.org/2012/08/here_comes_mcbr063131.html

It isn't easy to quantify the exact percentage of transposable elements that have been established to have some function because that number is steadily increasing -- it is thus a moving target. McBride is correct, however, that functions have not yet been identified for the majority of those transposable elements. But do we have sound reason to think that functions will not be ascribed to these elements in the future? Wouldn't it be better to take a "wait-and-see" approach to the non-coding genomic repertoire? Remember the title of the paper I cited in my previous response to McBride: "From 'JUNK' to Just Unexplored Noncoding Knowledge: the case of transcribed Alus." To borrow a Darwinist cliché, give science time!

Even the famous icon beta-hemoglobin "pseudogene" may be functional:

http://www.evolutionnews.org/2013/04/an_icon_of_the_071421.html

It is _incredibly_ unscientific to call DNA of unknown function "junk." Talk about a science stopper. And to double down and be dogmatic about it is worse still.

I know exactly nothing about genetics but this has always been galling to me as well. How much better simply to say that we don't know why such-and-such DNA strand exists. But no, you almost never hear, at a popular level, that there are some glaring facts for which biological science has zero explanation. The answers are always said to be just around the corner when, of course, if you really don't have the answer then there is no way you could put even an approximate date on when that answer will be arrived at! The sociological reasons for this public chest-beating are obvious and don't need rehashing here.

The OP makes a valid point about Wnt3a but contains big errors, not all of which are Lydia's.

- Wnt3a is not a "gene for tails," and Lydia got that right. Wnt3a is part of (quoting the TalkOrigins site) an underlying developmental pathway. So, Wnt3a is part of a system that is used to grow tails, but it's also part of other signaling systems that do other things. By itself, the presence of Wnt3a in humans is not strong evidence for the presence of a tail-growing program in humans.

- The TalkOrigins piece incorrectly identified the effect of the mouse mutants as "decreasing gene dosage." This confused Lydia, who reasonably assumed that the writer of the TO piece was using current/correct scientific terminology. They weren't. What the mouse mutations do (and this is clear to a developmental biologist from the rest of the description in the TO piece and from the original literature) is decrease expression of the Wnt3a gene, in the tail. They found no evidence of mutation in the Wnt3a gene, and concluded (correctly, I'm sure) that the mutation affects regulatory elements elsewhere. Unfortunately, the authors of the 1996 paper (free to read online, follow link in TO piece) used the term 'gene dosage' in their title. I'm not sure why they did that -- maybe the term wasn't solidified into its current definition until after 1996. Genes & Development is a very good journal, so I don't think it was a mistake at the time.

This is important because the developmental genetics in the mouse show (unsurprisingly) that mutations can cause Wnt3a-mediated dysfunction in some tissues and not others, leading (for example) to weirdness in the tail but not elsewhere. In other words, the fact that Wnt3a controls several developmental processes does not mean that these processes can't be affected separately. Atavistic tails are readily explained by such well known facts of developmental biology.

- Lydia writes of Wnt3a, "It fulfills an important function in human development, so it isn't switched off at all." This is completely wrong. You couldn't have cells or organisms if thousands of genes weren't switched off in some places and times and not others. That's really basic developmental biology. In fact, it is likely that Wnt3a is switched off in human tails, and this would be easy to examine.

- Lydia refers to the human tail as a "spinal chord." She means the spinal cord, and her description is inaccurate. The human tail is composed of multiple tissues and is indistinguishable from other mammalian tails at the same stage of development. It is not a "spinal chord," or a spinal cord. It is a tail that is destroyed by programmed cell death.

It is reasonable to be confused about the intricacies of developmental genetics, and excusable to be unaware of the function of developmental regulatory elements that explain how Wnt3a could be separately controlled in tails, to build them (or not). But trying to explain away human tails is not so respectable.

I find it interesting that you (SFM) are so opposed to referring to the human "tail" as an extension of the spinal cord. Yet the coccyx, which appears to be what is left when the rest of the appendage (whatever we call it) has naturally regressed is the final segment of the vertebral column. If one looks at pictures of embryos in utero before the "tail" has regressed, or at time-elapsed pictures of its regression to the coccyx, it appears to be an extension of the spinal column. If you would prefer "spinal column extension" to "spinal cord," well and good. The interesting thing is that if you look at the public Facebook discussion on Nancy Pearcey's wall, you will find intelligent defenders of the "atavistic tail" hypothesis clearly stating that the "tail" extension that we _all_ have in utero is "a tail in healthy humans." Yet an extension of the spinal column is what they appear to be talking about. Or is your concern, perhaps, with the fact that in those infants in which it does not regress, who are born with a "true tail," there are also skin and hair follicles on the outside? Is that part of the morphology supposed to make the argument for an atavistic origin significantly stronger?

Now, as far as switched-off-switched-on: I'm certainly willing to learn more. Is your contention that WNT-3a is normally "switched off" completely but just in the cells of the extra human extension in utero and that this is what causes its regression normally? But that it is "switched on" in those cells both in tailed animals and in humans born with true tails? Would you specify a paper that shows strong evidence for that?

Moreover, since the gene has a function in humans in other parts of the body and in development, and since the mechanism whereby (on your own account, if I have understood that account correctly) it is switched on in certain cells is peculiar to the individual, is not the argument for an atavistic origin undermined in any event? Remember that Giberson implied strongly that there is "junk" here, but even on your own account, WNT-3a is not "junk" but is simply accidentally not "switched off" in certain cells of the human body at a certain point in development. While still needed in other places and for other purposes. The argument from that to common descent is, in my view, quite weak. And that is even given that your own correction is accurate.

Let us recall, as well, that it apparently often happens that this individual event (a mutation or whatever it might be) in the individual human infant that causes the non-regression of the "tail" is accompanied by other medical problems. Which in my opinion is yet further evidence against the "atavism" view. In fact, the "atavism" claim seems like an explanatory fifth wheel no matter how one slices it.

Casey Luskin makes an argument against the "switched-off" claim even in the cells of the spinal column extension. (Emphasis added.)

During normal human embryogenesis, a "tail"-like structure appears around the fourth or fifth week of development. This isn't the result of vestigial genes that are normally "turned off" (as Giberson puts it) being accidentally turned back on when our development regresses to some primitive state. Rather, they are always and normally "turned on," and the formation of this tail-like structure is part of the normal process of the development of the human body plan and nervous system -- a point supported by the fact that the human embryonic notochord and neural tube are thought to extend through much if not all of the entire extent of the human embryonic tail.15 By the fifth or sixth week the "tail" reaches its full extent, but during the seventh and eighth week of development, it is reabsorbed into the embryo. By the end of the eighth week, the tail is usually completely gone.16

It's worth noting that the tail is not unusual or unique in being a structure that temporarily appears, and then disappears, during our development. A paper in Annals of Anatomy recognizes, "During normal human development a number of transient structures form and subsequently regress completely," and notes: "One of the most prominent structures that regress during development is the human tail."17 The paper goes on to explain that it is not unusual for cells or even macrostructures to die: "In the process of development and in adult life, large numbers of cells are known to die in many different tissues. In some cases, whole regions or entire organs are eliminated."18

http://www.evolutionnews.org/2014/05/do_human_tails_085451.html

And to clarify: What I meant by "isn't switched off at all" was "isn't switched off, period" or "*isn't* switched off [emphatic]." Giberson's implication is that WNT-3a is a "gene for tails" and is not functioning, is simply "switched off" in humans who are not born with tails. I find it rather intriguing to note that someone as well-informed as SFM should not be more concerned about the fact that Karl Giberson is going around telling people that humans sometimes are born with tails because the "gene for tails" which is usually "ignored" and "switched off" is "switched on" in those humans. Shouldn't this inaccuracy bother him? I don't know, maybe SFM has written privately to Karl Giberson telling him that he shouldn't be saying that. I would suggest it.

Again, WNT-3a cannot just be "switched off" in most of us or it wouldn't be doing stuff. I did not mean to imply that all genes are switched on in all tissues. What I did mean to imply is that saying that WNT-3a is normally switched off in humans is highly misleading. Even if it were true (which SFM says is likely but which Casey's point concerning neural tube extension tells against) that WNT-3a is switched off in the normal, transient human spinal column extension, Giberson's statements would be highly misleading and would make the case from this feature for common descent sound stronger than it is. It's an attempt to apply the junk DNA and "bad design" meme in a place where it does not even remotely begin to fit. That being the go-to argument for many on common descent, I suppose the reflex is understandable. But as far as I can see, as a layman, it won't wash here--not even close, and not even on SFM's version of the theory.

Hi Lydia, just some quick responses.

- The human tail is a tail. Calling it an extension of the "spinal chord" is wrong, and calling it an extension of the spinal column is accurate but misleading (IMO), unless we want to refer to a mouse tail in the same way. I guess I don't understand why it is reasonable or desirable to refer to the human tail in such terms. I propose using clear and straightforward language that would not lead a reader to conclude that humans don't have a tail.

- Yes, we completely agree that Wnt3a is not 'junk,' nor is it a genetic atavism.

- You ask, "Is your contention that WNT-3a is normally 'switched off' completely but just in the cells of the extra human extension in utero and that this is what causes its regression normally? But that it is 'switched on' in those cells both in tailed animals and in humans born with true tails?" No, Wnt3a is not switched off throughout a human embryo -- it is (as far as we know) expressed in various tissues that you have already accurately discussed, namely the developing nervous system. In mice, it is strongly expressed in the tailbud, and mutations that affect this expression affect the tail. Humans have a tail that regresses, and persistence of the tail is known to occur. (There is recent evidence that suggests, strongly to me, that persistence of the tail is more common than previously supposed -- tails are sometimes seen in midgestation by sonography, correlated with scars in the newborn at the presumptive site of resorption.) Therefore, scientists have reasonably postulated that disruptions in Wnt3a expression could underlie tail persistence in the human.

As I said in my last comment, verifying Wnt3a expression in the human tailbud would be easy to do, but I don't know if this has been reported. No developmental biologist would consider it surprising to see Wnt3a expression in the tailbud. The interesting question is whether such expression is turned off at the key time. That is also an easy thing to do, technically. I think the issues with obtaining samples should go without saying.

But the basic hypothesis here is that Wnt3a directs tail formation in the human, as it does in all other tailed animals examined so far. Then the tail regresses, and this is likely because Wnt3a expression is switched off. I say 'likely' here, but there are other possibilities, based on what we know about the tail-growing genetic program in other species. One interesting possibility (unlikely, IMO) is that a "tissue-destruction program" is switched on in ape tails, overriding the tail-growing program without turning it off, perhaps directed by the same tail-specific genetic cues that direct the tail-making program. That's a fine hypothesis, but it's just a hypothesis at this point (AFAIK).

- A persistent human tail is unquestionably atavistic, and noting that its genetic underpinnings involve genes with other roles is completely immaterial to the question of atavism. So, while we agree that it's incorrect to call Wnt3a a gene for tails, it is obviously true that the tail-growing program is conserved in humans, that the tail is removed under yet-unknown influences, and that a persistent tail represents retention of an ancient mammalian feature that is normally deleted in apes.

- Casey Luskin's description in the paragraph you quote is pretty good, but contains one significant error, which I've already mentioned. He writes, referring to Wnt3a and other tail-growing genes, "they are always and normally 'turned on'." That's wrong, and not even close to right. There are relatively few genes that are "always and normally turned on," and Wnt genes are notable in that they cannot be on all the time for an embryo of any kind to develop. Again, we don't know whether Wnt3a is turned off in the human tail, leading to its demise, but we sure do know that it's not turned on all the time.

- Atavisms are not, IMO, "evidence for common descent." They are observations that make sense in light of common descent, but make no sense under simplistic "design" arguments. I put "design" in scare quotes not to insult those ideas at all but to indicate that there may be robust design-based arguments that could make some sense of atavisms but that I have not seen. A design-based explanation for chicken teeth, human tails, and snake legs would need to be sophisticated and comprehensive, acknowledging (rather than trying to linguistically erase) their existence and providing explanation consistent with the assumptions made. I don't think this has been done effectively, and I doubt that it can, but hey: never say never.

Hope that was helpful/informative, really have to go.

calling it an extension of the spinal column is accurate but misleading (IMO), unless we want to refer to a mouse tail in the same way. I guess I don't understand why it is reasonable or desirable to refer to the human tail in such terms.

I would use some such phrase because it normally regresses. And, yes, it looks to me like it would be accurate to say that other mammalian tails are also extensions of the spinal column but that we call them "tails" because they are normal and functional organs of that mammal. They aren't normal in humans. What's normal in humans is the regression of that portion of the spinal column, which is why I think it makes perfect sense to call it an extension of the spinal column. All the more so in a conversation where we are trying not to prejudge the issue of whether or not it is an atavism, where that is the question at issue. (More on that in a moment.) All that being said, you will see that throughout I sometimes use the word "tail" with quotation marks and even sometimes without. I think "extension of the spinal column" sounds like about the most neutral phrase in this context, perhaps with "normally transient" at the beginning to describe it in humans.

By the way, I left my typo "chord" in the main post because I didn't want to play silly games of pretending I hadn't made a typo. But y'know, it's going to start looking a little childish if you keep bringing it up in comment after comment as though it's something more significant than a typo. That kind of archness tends to backfire on the one using it.

A persistent human tail is unquestionably atavistic, and noting that its genetic underpinnings involve genes with other roles is completely immaterial to the question of atavism.

What? I'm trying to wrap my brain around the term "unquestionably" here. Or even around how you might or must be using the term "atavistic" so that you can apply the adjective "unquestionably" to it. You _seem_ to be saying that it is somehow rationally impossible to doubt that the fact that some babies are born with tails, that the extension of the spinal column fails to regress in them, is a result of common ancestry. If that's your position, I'm here to tell you that you are wrong. It's completely possible to be a rational human being, to look, yea, verily, even at Karl Giberson's arguments, even at TalkOrigin's arguments, and even at what you have said, and still to have doubts of that conclusion.

If you think that noting that its genetic underpinnings involves a gene or genes with other roles is so completely immaterial argumentatively, perhaps you could reflect on how much stronger Karl Giberson makes the case appear by implying that that is not the case. I suggest that you re-read the main post and see how his "bad design" claim relies on his "not used" and "shut down" and "ignored" claim regarding the relevant gene.

Moreover: Note that TalkOrigins says (and you seem to confirm) that the exact cause of a particular human's failure of tail regression is unknown; however, TO implies that it is particular to the individual. That is, a specific mutation or even environmental factor. That, combined with the common finding of other problems in such infants, makes the use of a term like "birth defect" quite legitimate and also makes the assumption of common descent explanatorily otiose. We have a regulatory gene. It's doing good work for us. Sometimes, it looks like, an individual accidentally either get an excess gene dosage of it or (on your theory as I'm now interpreting it) it gets switched on in some cells at some point in development during which time in development it should be switched off in those cells, and then we get failure of tail regression and often other problems. The idea that common descent or "atavism" is fulfilling a robust explanatory role here seems to me obviously false. And understanding its falsehood is, yes, enhanced by understanding something of the value and function of that gene for normal human development.

Atavisms are not, IMO, "evidence for common descent." They are observations that make sense in light of common descent, but make no sense under simplistic "design" arguments.

I can't help wondering if you have some unusual definition of "evidence," since your second sentence would, on an explanatory model, imply that they are, indeed, evidence for common descent.

There are relatively few genes that are "always and normally turned on," and Wnt genes are notable in that they cannot be on all the time for an embryo of any kind to develop.

That's pretty obviously a grossly uncharitable interpretation of what Luskin meant. He meant, I take it, "normally and always turned on" during the relevant time period of human development and in the tissues under discussion. The immediately following sentences concerning notochord and neural tube extension confirm this interpretation.

Lydia,
The discussion seems to have moved to semantics and opinions about belief and plausibility. I'm not interested in pursuing those topics, so I will bow out after offering my sincere apology for peeving you with my unnecessary repetition of your typo. Be well.

All the best to you, too. and apology accepted.

Btw, I really should have worded what I said above more strongly, and that might perhaps have shown that I was not merely raising a semantic issue: To say that "A persistent human tail is unquestionably atavistic" is, in this context, either question-begging or foot-stomping, whichever one prefers to call it. An atavism, as I understand it, in the context of origins and evolution is the reemergence of a trait that used to belong to an organism's ancestors, where that later emergence is supposed to happen in some sense because that trait belonged to the organism's ancestors. That is precisely the question at issue here--whether or not the birth of babies with tails is an atavism. Therefore, it does not produce any progress, and it does not provide any evidence, merely to say that that attribution is unquestionable.

Concerning DarwinDefender shrieking about "eliminative arguments" --

In fact, logical reasoning is mostly "eliminative": the proper use of logic is much more able to identify falsehood than truth. So, what the DarwinDefenders are insisting is something like this:

1) No fair! You're using logic to test whether our cherished assertions are illogical (and thus false in some way or another);

2) Unless you can give us a new "explanation" that we will accept, it doesn't matter whether you show our cherished "explanation" to be illogical or irrational.

--------
Concerning this sort of accusation: "... the best they have is to just look at something and shrug and say "I don't see how evolution could have made that"."

What the DarwinDefenders mean by this is that personal credulity is superior to skepticism ... provided the personal credulity breaks in favor of Darwinism.

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