Since posting our recent rebuttals to the TalkOrigins page on the Cambrian explosion (see here and here), we’ve received some requests to respond to other pages on the TalkOrigins archive. One of these is a page purporting to respond to the claim that “Evolution cannot cause an increase in information.”
Of course this title equivocates on the meaning of “information.” As explained here, evolutionary mechanisms can generate new Shannon information, but that is often a trivial accomplishment and doesn’t at all necessarily mean you’ve generated any new functional biological feature. A random, garbled, functionless stretch of DNA can entail new “information” in the Shannon sense, but that’s never going to explain how complex functional biological features arise. In any case, the TalkOrigins page responds as follows:
It is hard to understand how anyone could make this claim, since anything mutations can do, mutations can undo. Some mutations add information to a genome; some subtract it.
That bizarre statement reflects a gross misunderstanding of how Darwinian evolution works. A longstanding postulate in evolutionary biology, called Dollo’s Law, holds that Darwinian evolution is often not reversible. Perhaps in some cases mutations can “undo” anything they “can do,” but it’s not at all clear that this is always the case.
There’s a good reason for Dollo’s Law. Darwinian evolution tends only to fix traits in a population when they confer some advantage upon the organism. Evolutionary biologist Jerry Coyne affirms this when he states: “It is indeed true that natural selection cannot build any feature in which intermediate steps do not confer a net benefit on the organism.”1 So some mutations might provide an advantage, but “reversing” those mutations would presumably cancel the advantage. As far as the Darwinian mechanism is concerned, there isn’t always a reason to expect that a mutation that “undoes” some advantageous trait will confer an advantage, get passed on to offspring, and be maintained in a population. So anything a mutation does cannot always be undone.
There’s another problem with TalkOrigins’ statement. It’s not very impressive to learn that mutations can “undo” — or break down — some structure. Proponents of intelligent design aren’t asking how complex structures can degrade, but rather how complex structures can be built in the first place.
In the quotation from Jerry Coyne above, he claims he knows of no case where a structure could not be built by intermediate steps where each step individually conferred an advantage on the organism. But proponents of intelligent design find that the data suggest many structures might in fact not be evolvable by Darwinian evolution–especially when multiple mutations are needed to convey any advantage on an organism.
In 2004, Michael Behe co-published a study in Protein Science with physicist David Snoke showing that if multiple mutations were required to produce a functional bond between two proteins, then “the mechanism of gene duplication and point mutation alone would be ineffective because few multicellular species reach the required population sizes.”2 In 2008, Behe and Snoke’s critics tried to refute them in the journal Genetics, but failed. The critics found that, in a human population, to obtain only two simultaneous mutations via Darwinian evolution “would take > 100 million years,” which they admitted was “very unlikely to occur on a reasonable timescale.”3 It’s becoming increasingly clear that many such “multi-mutation features,” which would require multiple mutations before providing any benefit, are likely to exist in biology.
Douglas Axe demonstrated the inability of Darwinian evolution to produce multi-mutation features in a 2010 peer-reviewed study. Axe calculated that when a “multi-mutation feature” requires more than six mutations before giving any benefit, it is unlikely to arise even in the whole history of the Earth.4 He provided empirical backing for this conclusion from experimental research he earlier published in the Journal of Molecular Biology, finding that only one in 1074 amino-acid sequences yields functional protein folds.5 That implies that protein folds in general are multi-mutation features, requiring many amino acids to be fixed before the assembly provides any functional advantage.
Another study by Axe and Ann Gauger found that merely converting one enzyme into a closely related enzyme — the kind of conversion that evolutionists claim can easily happen — would require a minimum of seven simultaneous changes,6exceeding the probabilistic resources available for evolution over the Earth’s history. This data implies that many biochemical features are so complex that they would require many mutations before providing any advantage to an organism, and would thus be beyond the “edge” of what Darwinian evolution can do.
An empirical study by Gauger and biologist Ralph Seelke similarly found that when merely two mutations along a stepwise pathway were required to restore function to a bacterial gene, even then the Darwinian mechanism failed.7 The reason the gene could not be fixed was because it got stuck on a local fitness maxima, where it was more advantageous to delete a weakly functional gene than to continue to express it in the hope that it would “find” the mutations that fixed the gene.
This corroborates a 2010 review paper by Michael Behe in Quarterly Review of Biology which found that when bacteria and viruses undergo adaptations at the molecular level, they tend to lose or diminish molecular functions.8
The problem here, again, is that sometimes mutations can’t “do” what they can “undo”: sometimes it’s more advantageous in the short term to take a path that leads away from a complex structure, even if that structure would lead to a significant advantage.
The take-home message here is that the ID movement is producing both empirical and theoretical research showing that when multiple mutations are required before conferring any advantage on an organism, the “waiting time” for those mutations is often beyond the time available over the entire history of the Earth. There are good reasons to expect that random mutations cannot build many complex features we see in biology. Some non-random process that can “look ahead” and find complex advantageous features is necessary.
TalkOrigins’s 3000 Unnamed Papers Citation Bluff
Another problem with the TalkOrigins page is that it cites some very weak data to back up its claims.
For example, one study that is cited pertained to the origin of RNASE1B, a digestive enzyme in a leaf-eating colobine monkey, the douc langur.9 The study claimed to re-trace a hypothetical pathway of about nine mutations which, in a somewhat stepwise fashion, could have provided a digestive advantage.
What really happened is that some (though not all) of the amino acid changes lowered the optimal pH for enzyme activity from 7.4 to 6.3. Both before and after this alleged evolutionary sequence, the enzyme performed the same function: breaking down RNA. So while part of this hypothetical sequence of mutations might have occurred by Darwinian evolution, there’s no evidence that anything new arose. This is small-scale evolution and does not solve the problem of evolving multi-mutation features.
In another study, the TalkOrigins Page states, “Yeast was put in a medium with very little sugar. After 450 generations, hexose transport genes had duplicated several times, and some of the duplicated versions had mutated further.” Assuming the description is correct, we see more of the same — nothing “new” is evolving. The key to gene duplication isn’t explaining how you can get more of the same, but rather how you can get something that wasn’t there before.
Finally, the page suggests searching for “gene duplication” on PubMed to find “more than 3000 references” on the topic. These papers, we’re meant to assume, show how evolutionary mechanisms can create new information. But a survey of major review articles on gene duplication I published here on ENV in 2010 revealed that the studies never established that mutations could have produced the complex features in question. After taking a close look at this literature, I found:
The NCSE’s (and Judge Jones’s) citation bluffs have not explained how neo-Darwinian mechanisms produce new functional biological information. Instead, the mechanisms invoked in these papers are vague and hypothetical at best:
- exons may have been “recruited” or “donated” from other genes (and in some cases from an “unknown sou[r]ce”);
- there were vague appeals to “extensive refashioning of the genome”;
- mutations were said to cause “fortuitous juxtaposition of suitable sequences” in a gene-promoting region that therefore “did not really ‘evolve'”;
- researchers assumed “radical change in the structure” due to “rapid, adaptive evolution” and claimed that “positive selection has played an important role in the evolution” of the gene, even though the function of the gene was unknown;
- genes were purportedly “cobbled together from DNA of no related function (or no function at all)”;
- the “creation” of new exons “from a unique noncoding genomic sequence that fortuitously evolved” was assumed, not demonstrated;
- we were given alternatives that promoter regions arose from a “random genomic sequence that happens to be similar to a promoter sequence,” or that the gene arose because it was inserted by pure chance right next to a functional promoter.
- explanations went little further than invoking “the chimeric fusion of two genes” based solely on sequence similarity;
- when no source material is recognizable, we’re told that “genes emerge and evolve very rapidly, generating copies that bear little similarity to their ancestral precursors” because they are simply “hypermutable”;
- we even saw “a striking case of convergent evolution” of “near-identical” proteins.
To reiterate, in no case were the odds of these unlikely events taking place actually calculated. Incredibly, natural selection was repeatedly invoked in instances where the investigators did not know the function of the gene being studied and thus could not possibly have identified any functional advantages gained through the mutations being invoked. In the case where multiple mutational steps were involved, no tests were done of the functional viability of the alleged intermediate stages. These papers offer vague stories but not viable, plausibly demonstrated explanations for the origin of new genetic information.
I haven’t gone through all “3000 references” cited by TalkOrigins. Neither, in all likelihood, has the author of the TalkOrigins page. But my strong suspicion is that if you went through many of those pages, you’d reach the same conclusion.
This 3000-unnamed-paper citation bluff — and much other material on this TalkOrigins page, are not to be taken seriously.
[1.] Jerry Coyne, “The Great Mutator,” The New Republic (June 14, 2007).
[2.] Michael Behe and David Snoke, “Simulating Evolution by Gene Duplication of Protein Features That Require Multiple Amino Acid Residues,” Protein Science 13 (2004): 2651-2664.
[3.] Rick Durrett and Deena Schmidt, “Waiting for Two Mutations: With Applications to Regulatory Sequence Evolution and the Limits of Darwinian Evolution,” Genetics 180 (2008):1501-1509.
[4.] Douglas Axe, “The Limits of Complex Adaptation: An Analysis Based on a Simple Model of Structured Bacterial Populations,” BIO-Complexity 2010 (4): 1-10.
[5.] Douglas Axe, “Estimating the Prevalence of Protein Sequences Adopting Functional Enzyme Folds,” Journal of Molecular Biology 341 (2004):1295-1315; Douglas Axe, “Extreme Functional Sensitivity to Conservative Amino Acid Changes on Enzyme Exteriors,” Journal of Molecular Biology 301 (2000): 585-95.
[6.] Ann Gauger and Douglas Axe, “The Evolutionary Accessibility of New Enzyme Functions: A Case Study from the Biotin Pathway,” BIO-Complexity 2011 (1): 1-17.
[7.] Ann Gauger, Stephanie Ebnet, Pamela F. Fahey, and Ralph Seelke, “Reductive Evolution Can Prevent Populations from Taking Simple Adaptive Paths to High Fitness,” BIO-Complexity 2010 (2): 1-9.
[8.] Michael Behe, “Experimental Evolution, Loss-of-Function Mutations, and the “First Rule of Adaptive Evolution,” The Quarterly Review of Biology 85(4) (December, 2010).
[9.] Jianzhi Zhang, Ya-ping Zhang, and Helene F. Rosenberg, “Adaptive evolution of a duplicated pancreatic ribonuclease gene in a leaf-eating monkey,” Nature Genetics, Vol. 30:411-415 (April 2002).