In five previous articles (find the full series here), I offered a series of responses to YouTuber Dave Farina’s criticisms of my defense of biochemist Michael Behe’s work. Here, in this final installment, I will engage with Farina’s comments regarding my defense of Behe’s most recent book, Darwin Devolves.
Farina remarks,
Finally we get to the fourth one, which is about Behe’s third and arguably dumbest book, Darwin Devolves. This is the one that botches super basic concepts in genetics so badly that it becomes painfully obvious that Behe is lying… the entire book is based on the singular insane lie that mutations “degrade information” in the genome and are somehow destructive. Of course this is meaningless, and simply meant to take advantage of people who have no idea what mutation means or even what DNA is.
This is a caricature of Behe’s thesis. Behe does not claim that all mutations are harmful to the organism. Indeed, most mutations are in fact neutral, a point Behe happily acknowledges in his book (see for example pp. 96-98 of Darwin Devolves where Behe states “neutral mutations are the bulk of changes at the molecular level”).1
Rather, Behe’s thesis is that beneficial mutations (which account for a small minority of all mutations) are heavily biased toward loss-of-function — that is, degradation of existing genetic information. This thesis is not just correct, but supported by extensive data from population genetics. There are vastly more ways to gain an advantage by breaking functional genetic elements than there are ways to gain an advantage by building a new, complex feature.
Finding the Destructive
Therefore, natural selection will always “find” the destructive, but beneficial, mutations (of which there are many more in number) long before it “finds” the constructive beneficial mutations (which are far rarer). This presents a formidable challenge to the idea that complex organisms have arisen from a simple single-celled progenitor, via entirely unguided processes.
Farina continues,
Even with simple point mutations, which don’t “degrade” anything, they just potentially alter the products of gene expression, the results are varied. But more importantly, there are large-scale mutations that I mentioned in the Behe debunk, like gene duplication and neofunctionalization, as well as de novo genes, which produce completely new proteins without losing any genetic material or existing functionality. Every biology undergraduate student in the world knows this.
Nobody in this debate is denying that constructive mutations, gene duplications, and de novo (i.e., taxonomically restricted) genes exist. Rather, Behe’s argument in Darwin Devolves is that beneficial mutations are heavily biased towards degradation or loss-of-function.
A Fundamental Problem
This is an empirical fact. There are vastly more ways to acquire an advantage by breaking a gene than there are to do so by building a genuinely new function. The implication of this fact must not be lost: blind evolution via random mutation and natural selection will tend to break or diminish functions at a much faster rate than it builds them. This means Darwinism faces a fundamental problem. A majority of gene duplications are lost to purifying selection or become pseudogenes. Successful neofunctionalization depends on a series of specific mutations that confer novel selectable function while preserving the original copy. In bacteria in particular, there is a significant time limit for neofunctionalization to occur since there is an energetic cost in carrying and transcribing a broken gene.2,3
In the case of de novo genes, their envisaged origin from non-coding DNA is typically assumed rather than demonstrated. Requirements for this to work include a functional open reading frame, a promoter, proper level and timing of expression, correct protein folding, and integration into existing cellular networks.
Citing mechanisms known to every undergraduate does not address the quantitative data, emphasized by Behe and others, on the rarity of constructive change relative to degradative change.
Repeating a Strawman
Farina goes on,
Let’s see how little Jonny tries to play it off. First, he tries to cover up the fact that Behe himself provided a counter-example to his own thesis with the C-Harlem variant of hemoglobin, and this mess is how he tries to do that: “Surprisingly, however, the C-Harlem gene, which builds directly on the foundation of the sickle gene and would entirely eliminate the drawbacks of the sickle mutation, has not yet turned up in Africa, where it would do the most good.” The reason for this is that the move from regular hemoglobin to C-Harlem would require two co-dependent mutations, whereas the sickle-cell trait requires only one.
Again, we see Jonny’s strategy of “ignore the critique and say something unrelated,” which almost always turns out to be some variant of “but it’s really unlikely!”
That doesn’t matter. Behe’s whole argument is based on the idea that non-reductive beneficial traits never evolve. But here we have an example of such a trait that he himself described in his book.
How frequently we expect it to evolve is completely irrelevant to the question of whether it exists.
And if we want to take this non-response seriously, it clearly evolved at least once, since we’ve documented its existence. Then he whines about Cit+ again, and says literally nothing.
Again, Farina is repeating a strawman. Behe does not claim that no constructive traits evolve. Rather, the claim is that beneficial mutations are biased in favor of degradative changes rather than constructive ones. Farina did not address my remarks on C-Harlem from the previous article — the article he is supposed to be responding to. So, I shall simply repeat what I wrote there.
The C-Harlem example supports Behe over Farina. As Behe explains in The Edge of Evolution, “Hereditary persistence of fetal hemoglobin (HPFH) is already widespread in Africa, ameliorating the problems of the sickle gene.”4 Surprisingly, however, “the C-Harlem gene, which builds directly on the foundation of the sickle gene and would entirely eliminate the drawbacks of the sickle mutation, has not yet turned up in Africa, where it would do the most good.”5 The reason for this is that the move from regular hemoglobin to C-Harlem would require two co-dependent mutations, whereas the sickle-cell trait requires only one.
The probability of getting the sickle-celled trait in any individual is about one in a hundred million. Assuming a population size of a million people, it should thus be expected to arise spontaneously approximately every hundred generations, which is within the reach of evolutionary processes. For the two necessary mutations needed for hemoglobin C-Harlem to occur at the same time, the probability is a hundred million multiplied by a hundred million, which is 1016. As Behe summarizes, “With a generation time of ten years and an average population size of a million people, on average it should take about a hundred billion years for that particular mutation to arise — more than the age of the universe.”6
Nonetheless, hemoglobin C-Harlem has arisen, and was first documented relatively recently in New York City.7 But this is because the initial sickle-cell trait was already adaptive, since it conferred resistance to the malarial parasite. Thus, natural selection can preserve the sickle-celled trait (requiring only a single mutation) first and then acquire the second mutation (building on the first), thereby giving rise to the C-Harlem trait, which confers an even greater advantage. The C-Harlem example, therefore, in fact supports Behe’s thesis rather than Farina’s.
A Disappointing Showing from Farina
Farina’s video response to my previous article series is characterized by misrepresentations of the literature he is citing, selective engagement with my own points, and reliance on insults and name-calling. He repeatedly and quietly drops major points on which he was shown to be incorrect.
Neither Behe, nor I, have ever denied the ability of evolution to produce small-scale adaptations, regulatory changes, or even occasional constructive mutations. Rather, we contend that there are definable limits to what the theory of evolution can accomplish. In particular, we would contend (and this is the main thesis of Behe’s book, Darwin Devolves) that most beneficial mutations involve degradation of existing information and that complex, integrated molecular systems can only be brought about by coordinated changes that exhaust the probabilistic resources afforded by population genetics.
Notes
- Behe, MJ. Darwin Devolves: The New Science About DNA That Challenges Evolution (p. 98). HarperCollins. Kindle Edition.
- Kuo CH, Ochman H. The extinction dynamics of bacterial pseudogenes. PLoS Genet. 2010 Aug 5;6(8):e1001050. doi: 10.1371/journal.pgen.1001050. PMID: 20700439; PMCID: PMC2916853.
- Gauger AK, Ebnet S, Fahey PF, Seelke R (2010) Reductive evolution can prevent populations from taking simple adaptive paths to high fitness. BIO-Complexity 2010(2):1-9.
- Behe MJ, The Edge of Evolution: The Search for the Limits of Darwinism (Free Press, 2007), 29.
- Ibid.
- Ibid., 110.
- Bookchin RM, Nagel RL, Ranney HM. Structure and properties of hemoglobin C-Harlem, a human hemoglobin variant with amino acid substitutions in 2 residues of the beta-polypeptide chain. J Biol Chem. 1967 Jan 25;242(2):248-55. PMID: 6016610.