From Why Evolution Is True, by everyone’s favorite University of Chicago atheist and evolutionary biologist:
A new paper in Proceedings of the National Academy of Sciences shows how a functional protein (an antifreeze protein in the blood of an Arctic fish) can be assembled out of scraps of genome that have no function at all. Moreover, the protein doesn’t become functional — e.g., being secreted into the fish blood to keep it from freezing — until the very last step of gene assembly, so the sequence looks “irreducibly complex”. But, contra the IDers, we can construct a perfectly naturalistic evolutionary sequence by looking at DNA in relatives and putative ancestors. This shows that the appearance of “irreducible complexity” — the existence of an adaptation that doesn’t seem to function until all its parts are in place — does not require a Behe-ian creationist Designer, but can arise from natural processes. But we already knew that.
Coyne is sure this is going to come as a rude shock, to our colleague and contributor Dr. Behe in particular, author of Darwin Devolves. It’s “a slap in the face of IDers like Michael Behe — a fish slap like the one below.” Here he links to a classic Monty Python gag. Brown University biologist Kenneth Miller likewise tweets about the PNAS article: “‘Intelligent Design’ lost in Kitzmiller v. Dover, but Michael Behe keeps trying to resuscitate it. Unfortunately, every year brings new examples of how novel genes arise not from ‘design,’ but from evolutionary mechanisms.”
Not So Fast, Gentlemen
Who, in fact, gets the fish slap? Coyne and Miller should read Evolution News more carefully. A couple of weeks ago Cornelius Hunter wrote about this very same paper, newly published in PNAS, “Molecular mechanism and history of non-sense to sense evolution of antifreeze glycoprotein gene in northern gadids.” Dr. Hunter asked, “At Last, the Details of How Proteins Evolve?” The answer: not quite. In fact, not at all.
[T]his week researchers at the University of Illinois announced ground-breaking research that provides a step-by-step, detailed, description of the evolution of a new protein-coding gene and associated regulatory DNA sequences. The protein in question is a so-called “antifreeze” protein that keeps the blood of Arctic codfish from freezing, and the new research provides the specific sequence of mutations, leading to the new gene.
Hunter writes: “[T]his new ‘research’ is, in actuality, a just-so story,” heavily dependent on serendipity.
The authors hint at this serendipity when they conclude that their story of how this protein evolved is an example of “evolutionary ingenuity.” Evolutionary ingenuity?
The press release is even more revealing. [Lead researcher Christina] Cheng admits that the evolution of this gene “occurred as a result of a series of seemingly improbable, serendipitous events.” For “not just any random DNA sequence can produce a viable protein.” Furthermore, in addition to the gene itself, “several other serendipitous events occurred.”
The DNA was “edited in just the right way,” and “somehow, the gene also obtained the proper control sequence that would allow the new gene to be transcribed into RNA.”
Even the evolutionists admit to the rampant serendipity. Nonetheless they are triumphant, for “the findings offer fresh insights into how a cell can invent ‘a new, functional gene from scratch.’”
In actuality the findings arose from a series of non-empirical claims. Fresh insights? Not so much.
An Often-Told Tale
What Jerry Coyne is talking about is actually a very old and less-than-overwhelming story about the evolution of an antifreeze protein in an Atlantic codfish. The tale started being told way back in the 1990s and this latest paper doesn’t add much that’s new, although it purports to find a non-functional stretch of DNA that may be a source for the repeated sequence. Folks in the ID movement have written about the story many times before.
For more at Evolution News, stretching back to 2010, see here:
- “A Fishy Story About Antifreeze Gene Evolution”
- “A Problem for Evolution Grows Worse: Brochosome Proteins Encoded By Orphan Genes”
- “Assessing the NCSE’s Citation Bluffs on the Evolution of New Genetic Information”
The Gene Evolution Game
In particular, note the “fishy story” post:
Sounds simple and compelling, right? Don’t be too impressed. If you go back and read my article, “How to Play the Gene Evolution Game,” you’ll find that by using a combination of three magic wands — Gene Duplication, Natural Selection, and Rearrangement — it’s a simple matter to concoct a just-so story to “explain” the origin of just about any gene sequence — no details required.
“This summary of these 3 simple rules of the Gene Evolution Game will help you explain anything:
“Gene Evolution Game Rule 1: Whenever you find sequence homology between two genes, just invoke a duplication event of some hypothetical, ancient ancestral gene, and you can explain how two different genes came to share their similarities.
“Gene Evolution Game Rule 2: When you need to explain how a gene acquired some new function, or evolved differences from another gene, just invoke the magic wand of natural selection. No need to demonstrate that there is any benefit to the new gene, or that a step-wise path to adaptation exists. Finally, natural selection is especially useful when part of your gene appears unique — since natural selection can change anything, just conclude that natural selection changed your gene so much that it no longer resembles its ancestor.
“Gene Evolution Game Rule 3: When a gene seems to be composed of the parts of several genes, just invoke duplications and rearrangements of all the DNA sequences you need, so you can get them all together in the right place. If you need to delete parts of a gene, or invert them, or transpose to a new location, just invoke different types of rearrangements as often and as liberally as you wish, and ba-da-bing, you’ve got your new gene!”
As I noted in “The Gene Evolution Game,” there are a number of important questions which should be addressed before a just-so story of genetic evolution can be made plausible:
- “Did the rearranged gene product … start out functional? If not, how quickly could it gain function? How was it preserved from loss until it became functional?
- Are proteins really as malleable as this story would suppose or would the new combined gene encounter folding or other contextual problems?
- What mutational pathway was taken to evolve Gene A … into a new gene with function B?
- What selective advantages were gained at each small step of this evolutionary pathway?
- Were any ‘large steps’ (i.e., multiple specific mutations) ever required to gain a selective advantage along the evolutionary pathway? Would such ‘large steps’ be likely to occur?
- Could all of this happen on a reasonable timescale?”
Alas, the paper addresses zero of these questions.
Precisely the same is true of the present study. More could be written about how this paper uses dubious rules but doesn’t adequately address the key questions. But that will have to wait for another occasion.
Photo: Christina Cheng, University of Illinois, by L. Brian Stauffer, via EurekAlert!