The flip side of the Galileo Gambit: Denyse O’Leary on multicellularity


Figure 7 from Anderson et al. 2016. Evolution of GKPID’s new function by unveiling a latent protein-binding site. (A) The binding surface for Pins in GKPIDs is derived from the GMP-binding surface of gk enzymes. Homology models of Anc-gkdup (left) and Anc-GK1PID (right) are shown as white surface, with all side chains that contact either GMP or Pins as yellow sticks. Pink sticks show GMP; green ribbon shows Pins backbone, with the side chains of all Pins residues that contact the GK protein shown as sticks. The phosphate group on GMP and on Pins residue 436 are shown as orange and red sticks. Black dotted lines, protein-ligand hydrogen bonds. In the AncGK1PID structure , substitutions at sites in the binding interface are shaded red, including key substitution s36P. The binding modes of extant gk enzymes and GKPIDs are similar and support the same conclusions (see Figure 7—figure supplement 1). (B) The structure of the hinge and GMP/Pins-binding lobes is conserved between the Pins-bound GKPID (blue, rat Dlg, 3UAT), the apo-gk enzyme (brown, S. cerevisiae guanylate kinase 1EX6), and the apo-gk-s36P mutant (gray, 4F4J), all in the open conformation.

Figure 7 from Anderson et al. 2016. Evolution of GKPID’s new function by unveiling a latent protein-binding site. (A) The binding surface for Pins in GKPIDs is derived from the GMP-binding surface of gk enzymes. Homology models of Anc-gkdup (left) and Anc-GK1PID (right) are shown as white surface, with all side chains that contact either GMP or Pins as yellow sticks. In the AncGK1PID structure , substitutions at sites in the binding interface are shaded red, including key substitution s36P. (B) The structure of the hinge and GMP/Pins-binding lobes is conserved between the Pins-bound GKPID (blue, rat Dlg, 3UAT), the apo-gk enzyme (brown, S. cerevisiae guanylate kinase 1EX6), and the apo-gk-s36P mutant (gray, 4F4J), all in the open conformation.

Cdesign proponentsists really don’t seem to like research on the evolution of multicellularity. Pretty much any time real scientists learn something new about the origins of multicellularity, writers on intelligent design blogs Evolution News & Views and Uncommon Descent feel compelled to tells why it’s wrong (for example, here, here, here, here, here, here, here, here, here, here, here, here, and here).

So I shouldn’t be surprised that Denyse O’Leary has weighed in on the latest work out of Ken Prehoda’s lab, in which Prehoda and colleagues identified a mutation crucial for forming and maintaining tissues in animals. Worse, from O’Leary’s point of view, the article describes the evolution of a new protein function, which is anathema to intelligent design thinkers. To say this post is badly argued is overly generous; it’s absolutely devoid of any substantive argument.

It begins “The Darwinian begins to sound like an overconfident historian,” and then quotes a Science Direct article on Prehoda’s research:

All it took was one mutation more than 600 million years ago. With that random act, a new protein function was born that helped our single-celled ancestor transition into an organized multicellular organism.

The next set of quotes is prefaced “But then notice how it all gets qualified.” It’s a rather long set of quotes, so I won’t paste it here, but check it out if you want to evaluate my claim: nothing in it ‘qualifies,’ in any important way, the claim in the block quote above.

The rest of the article is a mishmash of unsupported assertions, innuendos, and bad associations, starting with this:

I (O’Leary for News) was suddenly reminded of something I’ve been hearing all my life: Boastful claims about having solved an enigma of history. Who faked up Piltdown Man? comes to mind. It happened only a century ago, during a time of massive, mostly preserved, documentation, and we still don’t know.

This is the flip side of the Galileo Gambit, also known as “science was wrong before.” Come to think of it, an awful lot of what I read on ID blogs boils down to the same thing. Yes, science was wrong before, lots of times. That’s not evidence that it’s wrong on any particular point, and it’s especially not evidence that your preferred alternative is right.

Now, there is nothing wrong in principle with being an overconfident historian, provided other historians are allowed a kick at the can.

But no evidence is given (other than “science was wrong before”) that the “historians” in question are overconfident, and no one is preventing anyone from “having a kick at the can.” Is Denyse O’Leary not having a kick at the can with this post? Again, we see evidence of ID’s persecution complex.

The problem is that readers, absent that check and balance, get used to regarding evolution as a secular religion or philosophy. They think that they are closing in on The Facts because a scenario that sounds plausible to them has been provided.

Maybe. Maybe not.

No, if they actually read the article in question, they’ll think they’re closing in on the facts because the authors explain their methods and provide evidence that supports their conclusions. But don’t bother actually engaging the evidence, just throw out some non-arguments like “Maybe. Maybe not.”

That’s the problem with actually knowing a lot about evolution. It becomes a history, with all the baggage that history entails with respect to how firmly a conclusion can be drawn based on the evidence.

It was easier in the old days when the Darwin-in-the-schools lobby was just assumed in many quarters to be “right” in their every pronouncement. Knowing so much more now has changed all that.

Ah, the Darwin Lobby (or in this case, the subspecies Darwin-in-the-schools lobby), the Discovery Institute’s favored way of making scientists sound shady. We can translate that, roughly, to “people who spend their lives trying to advance our understanding of evolutionary processes.” Yes, science can be wrong, and when it is it’s usually science that figures it out. Sometimes, it’s by repeating an experiment and finding a different result. Sometimes, it’s by carefully reading a paper and pointing out flaws in methodology, assumptions, or analyses: The authors failed to apply a statistical correction for multiple comparisons. Their phylogenetic tree has poor bootstrap support at a critical node. One of the parameters of their model is at odds with empirical data. How it never happens is by simply asserting that a result could be wrong, while utterly failing to engage with the science.

I imagine someone at the Discovery Institute has requested the Prehoda lab’s original data, which they’re now reanalyzing after rigorous consideration of the best substitution model. They’re identifying flaws in the original methodology, which they’ll carefully avoid. They’ll send the manuscript to a legit scientific journal (i.e. not BIO-Complexity), where it will be peer reviewed and published after minor revisions, and then we’ll learn that the Prehoda lab’s results were, in fact, wrong.

Maybe. Maybe not.

Leave a Reply

Your email address will not be published. Required fields are marked *