Copy of Gauger's Gaffe!

Copy of http://marmotism.blogspot.com/2016/06/gaugers-gaffe.html by Bill Needle, in case the original disappears.

Casey Luskin Jr. David Klinghoffer recently alerted me (via Twitter) to an Ann Gauger article on EN&V entitled "The Placenta Problem: How Common Descent Fails".

Recall that Ann Gauger is allegedly a developmental biologist who (according to her Biologic Institute bio) "studied cell adhesion molecules involved in Drosophila embryogenesis". Apparently, being an alleged developmental biologist at the DI doesn't guarantee that you understand anything about biology. For example, near the beginning of her article Ann states the following:

According to the theory of common descent, all true mammals are supposed to have descended from a common ancestor with a placenta. This is a trait common to all mammals. However, it has been a puzzle for some time that placentas differ in the form they take among different mammalian clades.

Jebus! How clueless can you get?

Placentas are not common to all mammals. Monotremes, mammals that lay eggs (e.g. the platypus and four species of echidna), do not possess a placenta - but are still mammals. This basic biological fact seems to have eluded Dr. Gauger.

And this specific fact falsifies her opening statement above: the theory of common descent does not suppose that "all true mammals have descended from a common ancestor with a placenta". The existence of monotremes means that no actual scientist would make such a stupid statement.

Ann's attempt at setting up a creationist strawman argument fails spectacularly.

Or maybe I'm being too harsh on Ann. Maybe by "true mammals" Ann means eutherian mammals (so-called placental mammals). If not eutherians, what constitutes a "true mammal"? Is it the presence of a placenta? If so, then metatherians (marsupials) are also "true mammals" as they too utilize (at least relatively briefly) a placenta, albeit a yolk sac placenta (see here for a good description).

But I suspect, by erroneously stating that all mammals possess a placenta, Ann doesn't have a clue as to what she's talking about.

But let's set aside Ann's ignorance of basic biology.

The target of Ann's impotent creationist rage is recent actual scientific research that has discovered that mammals possess endogenous retrovirus (ERV) genes that are essential for placenta formation. That is, genes important for placenta formation appear to have been "captured" and repurposed from retrovirus genes. And the specific genes Ann cites are called syncytins. Here is a short description of syncytins from a 2015 paper (a paper Ann links to in her article) entitled "Retroviral envelope gene captures and syncytin exaptation for placentation in marsupials":

Syncytins are “captured” genes of retroviral origin, corresponding to the fusogenic envelope gene of endogenized retroviruses. They are present in a series of eutherian mammals, including humans and mice where they play an essential role in placentation.

What Ann appears to have a problem with (apart from ignorance of monotremes) is the evidence that indicates that syncytins vary between several mammalian groups. That is, all mammals do not possess the same syncytin genes for placentation. According to Ann (lack of italics Gauger's):

These "repurposed" proteins are called syncytins. They are essential for placental formation, yet are of independent origin in different kinds of mammals -- primates have one kind, mice another, rabbits, cows, and carnivores yet others. They are clade-specific. In fact, in 2015 a functional syncytin was found in several marsupials, extending the presence and essential function of the protein to all placental mammals examined. All syncytins are lineage-specific, meaning that each mammalian clade has its own syncytin, with a unique sequence and location in the genome. They must have inserted themselves (or been placed there) after the separation of the mammals into different clades! This means there must have been multiple independent acquisitions of these syncytins to participate in an essential process that is common to all mammals. Why should there be unique syncytins in each clade? 

Note that Ann does not define what she means by "clade". Clades are taxonomic groupings of organisms determined by phylogenetic relationships. Some clades are big, like phyla. Some clades are much smaller, like families and genera. Not all mammalian taxonomies agree on what to call various clades (e.g. infraclass or subfamily), but most taxonomies show congruence of various clades. The 2015 paper that Ann cites ("Retroviral envelope gene captures and syncytin exaptation for placentation in marsupials") provides a succinct figure depicting the major clades within the class Mammalia:

Note in the figure above that the syncytins so far identified in eutherian mammals are indicated by red arrows (those recently identified in marsupials are not).

So to give us some perspective, consider the syncytins found in humans (syncytin-1 and syncytin-2). In the diagram above, the hypothesized evolutionary appearance of these two syncytins is indicated on the line labeled "Haplorrhini". The Haplorrhini is a suborder of Primates that includes monkeys, apes, and humans. According to a 2013 paper entitled "Paleovirology of ‘syncytins’, retroviral env genes exapted for a role in placentation":

Comparative analysis of the syntenic regions within the genomes from various species revealed that the syncytin-1 gene entered the genome of primates before the separation of Hominoids from Old World monkeys, being conserved only in Hominoids, whereas syncytin-2 was found to be conserved in the genome of all primates, except prosimians.

Thus, sincytin-1 and syncytin-2 are genes shared by almost all primates including humans. How does one account for this? Can you say "common ancestry"? Syncytins are another piece of molecular evidence supporting the common ancestry of humans, apes, and other primates.

And I wouldn't have bothered reading up on syncytins if Ann hadn't tried to twist their existence into some sort of evidence for creation (she tries, you'll see). Thanks Ann!

Dr. Gauger then burbles this bit (again, lack italics, Ann's):

What we have to explain is the unique and independent group-specific cooption of syncytins for a function that is essential for placental development, a feature common to all mammalian groups. Six independent origins for the placenta! There is no evidence of a grand ancestral syncytin shared by all groups that was later replaced by other syncytins, so the common descent explanation of the placenta in mammals fails.

First, explaining the "unique and independent group-specific cooption of syncytins for a function that is essential for placental development" is exactly what actual scientists have done. Didn't Ann bother to read the 2013 and 2015 syncytin papers she links to in her article? It seems she hasn't. How predictable.

Second, differing origins of placental characteristics help to explain the fact that placental structure varies amongst eutherian mammal groups. According to the 2013 paper cited above:

Interestingly, comparative anatomy reveals that the placenta is the most variable organ among mammalian species (reviewed in Wooding & Burton; figure 5). Placentae essentially differ in the extent of uterine tissue invasion by the trophoblast cells covering the blastocyst at implantation and by the architecture of the resulting maternal–fetal interface.

The paper then briefly describes four different placental architectures that are referred to as the epitheliochorial placenta, the synepitheliochorial placenta, the endotheliochorial placenta, and the hemochorial placenta (humans have this version). Again, according to the 2013 paper:

[T]he degree of invasiveness of the trophoblast increases from one type to the next, respectively, and is accompanied by sequential loss of the intervening maternal cell layers (epithelial and endothelial cells), up to direct contact between the syncytiotrophoblast and maternal blood in the case of the hemochorial placenta (figure 5).

So, there is no one placental structure. I think Ann knows this (surprisingly), but she doesn't imply variation in placental structure anywhere in the first half of her article. And this is a bit deceptive.

Third, as stated earlier, all mammals do not have a placenta.

Fourth, ERV genes represent a type of transposable element (TE), and TEs are not exactly rare. According to the 2013 paper:

Altogether, these elements occupy a substantial fraction of many eukaryotic genomes. For instance, they make up at least 45% and 40% of the human and mouse genomes, respectively.

So, finding virally derived syncytins in the genomes of different mammals is not really surprising... to actual scientists.

And finally, Ann's last sentence in the above quote is not entirely accurate. You see, Ann inadvertently outlines a prediction based upon an hypothesis that would explain the fact that not all mammals share the same syncytins (or the same placental structure). According to the 2013 paper:

These genes of exogenous origin and acquired ‘by chance’ raise a paradox, as they are ‘necessary’ to carry out a basic function common to placental mammals, and yet they appear to have been acquired lately. Indeed, although the capture of some of them dates back to up to 80 Myr, the presently identified syncytins can still be considered as relatively recent genes by comparison with the date of emergence of a primitive placenta in a mammalian ancestor (approx. 150 Ma). To resolve this paradox, an evolutionary model can be proposed which is consistent with our present knowledge on the paleontology of retroviral elements, and the functional properties identified for the env genes, either from present-day infectious retroviruses or from anciently captured ERVs.

Imagine! A scientific model to explain observable data that is consistent with present knowledge. Scandalous!

And here's the proposed - and testable - model (from the 2013 paper):

The model states that a pivotal event in the emergence of placental mammals has been the capture of a founding retroviral env gene, but that this ancestral env gene has been subsequently replaced in the diverse lineages emerging in the course of the mammalian radiation upon successive and independent germline infections by new retroviruses and co-optation of their env gene, each new gene providing its host with a positive selective advantage (figure 5). 

So, the proposed hypothesis postulates an ancestral mammalian "syncytin" that has since been replaced, in similar ERV fashion, by more recent syncytins.

This proposed model accounts for some of the mammalian characteristics observed today (from the 2013 paper):

Such a hypothesis would account for the evolutionary transition from egg-laying to placental animals as well as for the diversity in both the nature and time of insertion of the captured syncytins that can be currently found. It would also rather simply account for the multiplicity of placental structures that have emerged, concomitantly with the diversity of the captured env genes.

This model also makes a very specific prediction that is supported by evidence that Ann implies doesn't exist (from the 2013 paper):

A consequence of this model is that evidence should exist for ‘lost syncytins’ in eutherian mammals, and this is precisely what was found in a recent study of another human envelope protein gene, belonging to a HERV-V provirus, named envV, which is also specifically expressed within the human placenta, and whose putative role in human placentation remains to be investigated since it was found to be non-fusogenic. 

According to Ann: "There is no evidence of a grand ancestral syncytin shared by all groups that was later replaced by other syncytins". Well, the "grand ancestral" syncytin may not have been discovered - yet. But evidence for "lost" syncitins that have subsequently been replaced has indeed been discovered. Thus, the proposed model explaining placental evolution is supported by actual evidence.

And a further point, remember - even though Ann is ignorant of this fact - not all mammals possess a placenta. The most primitive mammals, monotremes, lay eggs. Thus, placentas are not essential for the existence of Mammalia as a group. But with the evolution of placental structures, mammals evolved and radiated into marsupials and then into the so-called placental mammals. The model outlined above - and supported by evidence - explains this transition.

But Ann can't accept this model. It challenges her religious dogma scientific understanding. Thus, she proposes an alternative "hypothesis":

Common design has an explanation, but not one that will be palatable to my interlocutors. The designer used the same idea six different times to produce the same outcome in six different "designs" (clades). That's another way of saying all these clades have the same outcome, the placenta, but achieved by independent uses of the same idea. 

This can be stated as a general principle. Design predicts [Ann's emphasis] that we should find other examples where there are similar but independent ways of performing an essential function or of solving a common biological problem. The means may differ between groups, but the outcome is the same across groups. Or to put it another way, multiple independent paths converge on a common solution. There are many examples of this known already, at the molecular and organismal level. It's known in evolutionary terms as convergent evolution, but I'll call it convergent design.

The foremost problem with Ann's religiously motivated "hypothesis" is that it requires a god "designer" for which there is no scientific evidence. IDCers love to argue that a "designer" must exist because we allegedly see "design" in nature, and if we see "design" then there must be a "designer". "Reasoning" so painfully circular as to be completely useless.

The other major problem with Ann's "hypothesis" can be formulated in the question: "What would design not look like"? Because from Ann's description, everything would fit her "hypothesis". In other words, her "hypothesis" cannot be falsified, and therefore it is not testable, and it is not scientific. Her alleged omnipotent god "designer" could do whatever the hell they wanted, so anything and everything we find must be "designed". Her "hypothesis" explains nothing.

That nothing that Ann's "hypothesis" fails to explain is simply why:
Why did the "designer" design "six different 'designs'"?
Why did the "designer" not choose one design?
Why did the "designer" design mammals that lay eggs, or mammals with pouches, when seemingly placentas appear to be so superior?
Why did the "designer" make syncytins look indistinguishable from ERVs?

So many questions. Absolutely no answers. Not from Ann and her "hypothesis" anyway.

Essentially, Ann's "hypothesis" boils down to god the designer-did-it.

Fortunately, the evolutionary hypothesis presented above does explain why we observe what we observe. No omnipotent, magic god "designer" required.

In the end, the above scientific hypothesis regarding syncitins and placental evolution may or may not turn out to be correct. But either way, Ann's magical creation pseudo-hypothesis absolutely fails to account for what we observe.

The placenta poses no problem to common descent. Suck it Ann (you too, Klinghoffer).