Editor’s note: For previous replies by Dr. Gauger to Dr. Torley in this series, see here, here, and here.

Philosopher Vincent Torley (and Washington University’s Professor Josh Swamidass) have been trying to persuade me that common descent is the only rational view to affirm, the only intellectually consistent and respectable choice. What they don’t seem to realize is that I see the evidence for common descent. I know its strength. The reason I doubt common descent is not because of the ways that it succeeds, but the ways that it fails.

Writing at Uncommon Descent, Torley poses the following challenge in “Consider the Opossum,” thinking to trap me into either accepting the argument for common descent as the only evidence-based conclusion, or denying the evidence in order to escape the logic:

Do you accept that if hypothesis A readily explains an empirical fact F and hypothesis B does not, then F (taken by itself) constitutes scientific evidence for A over B? Or putting it another way, if a fact F is predicted by hypothesis A, and compatible with hypothesis B but not predicted by B, then do you agree that F constitutes scientific evidence for A over B? If not, why not?

Do I accept Torley’s logic? Yes. Do I think common descent is explanatory (A) and design is not (B)? No. Do I think that common descent is predictive (A) and design not (B)? No. The reason is that the syllogisms cut both ways. Design is both explanatory and predictive, particularly when dealing with pattern breaking observations in biology, where common descent doesn’t work as an explanation. Thus the onus of proof is not on design alone, as Professor Swamidass thinks, but on common descent as well.

Let me show you. 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.

In the year 2000, French researcher Thierry Heidmann and coworkers found that genes derived from endogenous retroviruses (ERVs) appear to have been coopted to perform an essential role in placental formation. These genes, which resemble the ERV envelope gene env, make a protein that originally promoted fusion of the virus with its host cell’s membrane, but now acts to promote fusion of membranes between the embryo and the lining of the uterus. 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?

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.

I repeat: distinct syncytins for cows, carnivores, rodents, primates, rabbits, and even tenrecs (a species thought to retain features of primitive mammals). We all recognize these clades based on their traits — cows are different from carnivores, which are different from rodents, which are different from chimpanzees. Even nursery school children can tell the difference. And they are all thought to have descended from a common ancestor, the proto-mammal. Well, apparently, these well-defined clades of mammals make their placentas using analogous but distinct proteins. This perhaps explains why the placentas of each clade differ in their structures. But it flies in the face of the idea that all mammals are descended from a single kind of ancestor with a single kind of placenta.

I’ll quote a review paper on syncytins. These are the people who discovered syncytins, and they have done great work. Yet they are forced into a corner by their own work and the idea of common descent. I have italicized the key features of syncytins that must be explained, and bolded the explanations offered:

… syncytins are ‘new’ genes encoding proteins derived from the envelope protein of endogenous retroviral elements that have been captured and domesticated on multiple occasions and independently in diverse mammalian species, through a process of convergent evolution. Knockout of syncytin genes in mice provided evidence for their absolute requirement for placenta development and embryo survival, via formation by cell-cell fusion of syncytial cell layers at the fetal-maternal interface. These genes of exogenous origin, acquired ‘by chance’ and yet still ‘necessary’ to carry out a basic function in placental mammals, may have been pivotal in the emergence of mammalian ancestors with a placenta from egg-laying animals via the capture of a founding retroviral env gene, subsequently replaced in the diverse mammalian lineages by new env-derived syncytin genes, each providing its host with a positive selective advantage.

Rather than postulating six independent, random capture events in placental development, they are now postulating at least one more, a founding syncytin leading to a primitive placenta, then the other syncytins to replace that one in each lineage. Each replacement must have had a clear selective advantage as time went on to make the replacement possible, and each must be the outcome of a random series of events. To say it again, the common descent prediction is that there must have been a founding syncytin in the first mammal with a placenta, or something else that functioned in syncytin’s place, in order for the primitive placenta to arise and subsequently be passed to all mammalian clades. For which there is no evidence, and may never be.

Can common descent explain the unexpected observation of six independent origins for the placenta? No. Could it predict it? No.

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 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.

Convergent design is to be expected under the design hypothesis because the designer is not constrained by an evolutionary tree. He can reuse ideas that work in one setting in a different place. In fact, he can mix and match his methods to get to any outcome he wants. I am thinking of echinoderms (sea stars and sea urchins) that look alike as adults but get there by very different developmental paths, or two very different animal groups that come up with similar molecular solutions to create a new function, echolocation.

Convergent design is clearly observable across biology but has no evolutionary mechanism. There are proposed reasons for it but no demonstration. I can hear in my head the arguments of evolutionary biologists: intrinsic constraints, canalization, living in similar environments or ecological niches, you have no demonstration either…

So then maybe the answer comes down to probability.

In considering these alternative explanations, ask yourself, how likely is it that a retrovirus would infect, invade the germ line (the cells that make eggs and sperm), then insert itself at random in locations in the genome that are expressed in the developing embryo or primitive uterus at the proper time, then promote fusion of membranes to permit the formation of a placenta, with all this happening at least six separate times in the six lineages tested so far? We should also make clear, expressing a syncytin by itself is unlikely to be enough to make a placenta, which is a complex organ requiring interactions between mother and embryo, and the ability to exchange nutrients and oxygen.

Let me close by posing Torley’s questions to him, concerning syncytins:

Do you accept that if hypothesis A readily explains an empirical fact F and hypothesis B does not, then F (taken by itself) constitutes scientific evidence for A over B? Or putting it another way, if a fact F is predicted by hypothesis A, and compatible with hypothesis B but not predicted by B, then do you agree that F constitutes scientific evidence for A over B? If not, why not?

Evidence for and against common descent. It’s not nearly so open and shut a case as some believe, unless there is an a priori commitment to materialistic explanations.

Photo credit: © poplasen — stock.adobe.com.