Wednesday, 28 June 2023
Correcting professor Dave on "Darwin devolves"
Answering Farina on Behe’s Work: Darwin Devolves
In three previous articles (here, here, andhere ), I began a series of four responses to You-Tuber “Professor Dave” Farina’s video review of Michael Behe’s three books. In this final post, I will turn my attention to Farina’s comments regarding Darwin Devolves.
Hemoglobin and C-Harlem
In Darwin Devolves, Behe contends that the majority of helpful mutations are deleterious rather than constructive, since there are far more ways to gain an advantage by breaking than by building something. Says the Farina video:
If Behe had bothered to look at some of the most well-documented examples of evolutionary change, he’d know that this isn’t the case. In fact, he should know this is nonsense based on examples he himself described in his other works. For example, in Edge of Evolution, Behe describes a hemoglobin allele called HbC-Harlem, which, similar to the allele that causes sickle-cell disease, confers resistance to malaria, with, as Behe describes, “the advantages but not the drawbacks of sickle.”
But this “example of evolutionary change” shows precisely the opposite of what Farina wants. 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.”1 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.”2 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.”3Nonetheless, hemoglobin C-Harlem has arisen, and was first documented relatively recently in New York City.4 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. It looks like Mr. Farina did not review this example very carefully.
Cit+ in E. coli
As Farina’s second example, he notes,
[Dr. Behe] also describes the aforementioned Cit+ trait in the E. coli of the LTEE [Richard Lenski’s long-term evolution experiment], which has a new metabolic option, without compromising any existing pathways, literally debunking himself yet refusing to acknowledge it.
I have already addressed this example (see here), so I will not belabor the point further. Suffice it to say that Behe discusses Lenski’s work at length in Chapter 7 of Darwin Devolves, and Farina fails to engage with anything Behe writes concerning the long-term evolution experiment.
De Novo Gene Birth
Another complaint in the Farina video is that,
As you are likely beginning to see, creationists [sic] have a sadistic obsession with painting evolution as some kind of destructive force, but to do so they have to ignore a long and expanding list of completely new genes rapidly evolving everywhere we look. There are many papers like this one examining the concept of de novo genes. These are new genes that originate when previously non-expressed DNA becomes protein-coding and preserved via natural selection due to promoters arising near previously non-coding sections of DNA. So, we have a section of DNA that was not a gene, which is now a gene. New genes. We used to think this was rare, but once we figured out how to look for them, by identifying protein-coding sequences that aren’t protein coding in all the most closely related species, we started finding them all over the place.
The review paper Farina cites, by Stephen Branden Van Oss and Anne-Ruxandra Carvunis, notes (as is common in review papers dealing with this subject) that, for a long time, “the consensus view was that virtually all genes were derived from ancestral genes, with Francois Jacob famously remarking in a 1977 essay that ‘the probability that a functional protein would appear de novo by random association of amino acids is practically zero’.”5 But “though de novo gene birth was once viewed as a highly unlikely occurrence, there are now several unequivocal examples of the phenomenon that have been described.”6 In other words, though it was once thought that the origins of fundamentally new genes from non-coding sequences was essentially impossible, the fact that we observe a plethora of taxonomically-restricted genes, rather than being taken as a disconfirmed prediction of evolution, is taken to show that de novo genes can be birthed by evolution quite readily after all. Evolutionary theory, remarkably, is taken to be completely insensitive to disconfirming evidence.
Moreover, though some examples of taxonomically restricted genes bear some resemblance to non-coding stretches of DNA in related species, this is not so with the majority of cases. Furthermore, there is no convincing mechanistic scenario by which non-coding DNA may be transformed into genes coding for proteins that are ready to fulfil a functional role.
Polar Bears
According to Farina,
Perhaps the best evidence that Darwin Devolves is nonsense is that Behe had to flat out lie to defend it. In a discussion of Behe’s treatment of documented adaptations in polar bears, Dr. Nathan Lents pointed out that Behe did not accurately represent the findings of a paper he cited, when he claimed that virtually all adaptations that polar bears have to their arctic climate are actually damaging in some way. In response, Behe provided a table from that paper, showing that all the documented mutations are either “possibly damaging” or “probably damaging.” But he must have thought nobody would check up on him, since Dr. Lents showed that Behe sneakily omitted two columns and many rows, and the omitted data, unsurprisingly, tell a very different story… Apart from the two restored columns, look at all those rows that say “benign,” meaning not harmful in effect. You know, the exact opposite of what Behe is claiming?
This claim has been rebutted thoroughly elsewhere (such as here). In brief, Behe nowhere denies that non-adaptive neutral mutations are common in evolution. Rather, his thesis is that the vast majority of positively selectedmutations are damaging, since there are far more ways for an organism to acquire an advantage by breaking something than there are ways to gain an advantage by building something new. In Darwin Devolves, Behe contended that “65 to 83 percent of helpful, positively selected genes are estimated to have suffered at least one damaging mutation.”7 Given that the entire chart from the Liu et al. paper, cited by Behe, is some 47 rows long and 8 columns wide, it made more sense to reproduce only the portion of the chart that was relevant to supporting his point. There is nothing duplicitous here. Behe omitted from the chart the data from the HVar algorithm (instead showing only the results of the HDiv algorithm) and also left out instances where the HDiv algorithm predicted that a mutation was benign. This served Behe’s purpose of confirming for his readers that up to 14 of the 17 genes examined (i.e., 83 percent) were probably or possibly damaging. The instances where a mutation was not predicted to be damaging (i.e., those listed as benign) do not contradict Behe’s thesis, since Behe never denied that many mutations are benign. Indeed, a significant majority of mutations are benign (e.g., the third codon position may be substituted without altering the amino acid sequence). But Behe’s thesis is that the vast majority of adaptive mutations (which make up a minority of mutations overall) are destructive rather than constructive. There is nothing in the chart that invalidates or undermines this thesis.
Conclusion
Farina’s video rebuttal directed at Behe’s work misrepresents Behe at multiple points. Moreover, Farina misreads several papers that he cites in his video, failing to understand how they intersect with Behe’s critiques of evolutionary theory. There is also little that is new to see in his video. Many of his criticisms of Behe have been made before by others and addressed in detail elsewhere. In short, despite Mr. Farina’s smug condescension and patronizing demeanor, he fails to mount a credible critique of Dr. Behe’s thesis.
Notes
Behe MJ, The Edge of Evolution: The Search for the Limits of Darwinism (Free Press, 2007), 29.
Ibid.
Ibid., 110.
Bookchin RM, Nagel RL, and 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. Journal of Biological Chemistry 1967; 242:248-255.
Van Oss SB, Carvunis AR. De novo gene birth. PLoS Genet. 2019 May 23;15(5):e1008160.
Ibid.
Behe MJ, Darwin Devolves: The New Science About DNA That Challenges Evolution (HarperOne, 2020), 17.
Correcting professor Dave on the "edge of evolution"
Answering Farina on Behe’s Work: The Edge of Evolution
In two previous articles (here and here), I began a series of responses to YouTuber “Professor Dave” Farina’s video about Michael Behe’s three books. In this essay, I turn my attention to Mr. Farina’s comments regarding The Edge of Evolution.
Malaria
In the video, Farina claims that “[Dr. Behe] seems to think that for any given biochemical trait, like drug resistance or disease immunity, there is one way, and only one way, to accomplish that job, despite he himself describing the biochemical details of more than one form of malaria resistance found in humans.” Actually, in The Edge of Evolution, Behe discusses the biochemical details of malarial resistance to two different drugs, namely, atovaquone and chloroquine. In regard to chloroquine resistance, Behe described the Plasmodium falciparum chloroquine resistance transporter, coded by the pfcrt gene, which is recognized to be of primary importance in conferring chloroquine resistance.1 This pump naturally functions as a peptide transporter. Mutations that enable the transporter to pump chloroquine impair its ability to pump peptides and actually entail a significant fitness cost to the parasite.2 As Behe explains in The Edge of Evolution, at least two co-dependent amino acid substitutions are necessary for this chloroquine resistance phenotype3 — and public health data suggests that it occurs approximately once in every 1020 cells.4 From this, it may be predicted that an adaptation requiring four co-dependent substitutions would arise in every 1040 malarial cells. Given that less than 1040 organisms have likely ever existed on earth5, this number is quite prohibitive. The challenge is even more acute when we are dealing with complex animals such as mammals, which have far, far fewer individuals. Until relatively recently, the effective population size of hominids, for instance, was only in the range of 10,000-20,000 individuals. If it is challenging for complex traits to evolve in single-celled organisms, it is much, much more difficult for them to evolve in more complex organisms. For a more detailed treatment of this subject, I refer readers to this article by Casey Luskin.
Farina contends that,
Behe butchers the concept of fitness landscapes in a way that is both extremely basic and completely undermines his argument…In one time or place, a particular genotype might be extremely fit, but in a different time or place, it might have low fitness. Behe completely misses this trivial detail. He argues that crossing “valleys” is impossible via evolutionary processes, since any intermediate between two peaks or two high-fitness genotypes will be low fitness, and selected against. In making this argument, he assumes that fitness landscapes are constant, and genotypes have fixed fitness values, regardless of environmental or ecological conditions.
But for many complex adaptations, such as those described in Behe’s books, a fitness benefit is not realized until multiple co-dependent mutations have arisen. A protein that stably folds, in order to mutate into a fundamentally different fold, will have to pass through a fitness valley where it does not stably fold and no longer performs its role. Such a protein will not be selected for under an alternative set of environmental conditions. It seems that, again, Farina fails to understand Behe’s argument.
Bizarrely, Farina asserts that “it’s quite amusing to note that if Behe considers [antimalarial] drug resistance to be impossible to evolve, it means that he believes in a god who deliberately bestowed plasmodia with resistance to our drugs in order to ensure that we continue to contract malaria. Gee, what a swell guy.” But this, too, betrays a misunderstanding of what Behe argues in The Edge of Evolution. He does not deny that malarial parasites have acquired resistance to chloroquine and other antimalarial drugs. Quite the contrary. Rather, as discussed above, he notes that malarial resistance to chloroquine has arisen and that it occurs approximately once in every 1020 cells. He then uses this data to extrapolate to a case requiring twice as many co-dependent changes to bring about, and he points out that this problem is far more acute in the case of more complex organisms like large mammals, with much smaller population sizes, longer generation turn-over times, and lower mutation rates.
Interestingly, this same misrepresentation of The Edge of Evolution was made by Nathen Lents in his review of Darwin Devolves (discussed by Casey Luskin here). This makes me wonder whether Farina has in fact read Behe’s book for himself, or whether he is relying upon others, such as Lents, for his information about what is in the book.
HIV
In his video, Farina takes issue with Behe’s claims concerning HIV that “there have been no significant basic biological changes in the virus at all” and “There have been no reports of new viral protein-protein interactions developing in an infected cell due to mutations in HIV proteins.”6 He cites the Vpu example discussed in part one. However, as Behe acknowledged years ago, this was one example he had overlooked in The Edge of Evolution. Nonetheless, it does not significantly impact the thesis of the book, since the statement may be modified to assert that “There have been hardly any reports of new viral protein-protein interactions developing in an infected cell due to mutations in HIV proteins,” despite the fact that “HIV has almost certainly altered its proteins at one point or another in the past few decades enough to cover all of shape space.”7 Behe does not deny that new protein-protein binding sites have arisen by mutations in HIV. In fact, he explicitly states that its mutated proteins must have bound many molecules, though “none seem to have helped it” such that they were preserved by selection.8 The reason for this is what Behe dubs the problem of restricted choice — “That is, not only do new protein interactions have to develop, there has to be some protein available that would actually do some good.”9 Vpu is one exception where it did apparently help. But given how much better an evolver HIV is relative to essentially any other organism (with its 109-1010 individual viruses per infected person and its mutation rate of 10-4, meaning that all possible double point mutations will arise in each virus in one individual every single day), the problem is certainly much more acute for other life forms.
Notes
Sidhu AB, Verdier-Pinard D, Fidock DA. Chloroquine resistance in Plasmodium falciparum malaria parasites conferred by pfcrt mutations. Science. 2002;298(5591):210-3.
Felger I, Beck HP. Fitness costs of resistance to antimalarial drugs. Trends Parasitol. 2008;24(8):331-3.
Summers RL, Dave A, Dolstra TJ, Bellanca S, Marchetti RV, Nash MN, Richards SN, Goh V, Schenk RL, Stein WD, Kirk K, Sanchez CP, Lanzer M, Martin RE. Diverse mutational pathways converge on saturable chloroquine transport via the malaria parasite’s chloroquine resistance transporter. Proc Natl Acad Sci USA.2014;111(17):E1759-67.
White NJ. Antimalarial drug resistance. J Clin Invest. 2004; 113(8):1084-92.
Whitman WB, Coleman DC, Wiebe WJ. Prokaryotes: the unseen majority. Proc Natl Acad Sci U S A. 1998; 95(12):6578-83.
Behe MJ, The Edge of Evolution: The Search for the Limits of Darwinism (Free Press, 2007), 139.
Ibid., 157-158.
Ibid.
Ibid., 157.
Nothing simple about these beginnings.
Gifted Microbes Elevate the Case for Intelligent Design to the Entire Biosphere
Far from being humble, primitive steppingstones to higher life, microbes display superpowers that so-called “higher” forms of life depend on. Here are some recent examples.
Never Say Forever
So-called “forever chemicals” known as PFAS (poly-fluoroalkyl substances) have been in the news as a pollution concern because they resist breakdown for decades in the soil and water. UC Riverside says that our lust for industrial applications comes at a price:
Chlorinated PFAS are a large group in the forever chemical family of thousands of compounds. They include a variety of non-flammable hydraulic fluids used in industry and compounds used to make chemically stable films that serve as moisture barriers in various industrial, packaging, and electronic applications.
The “unusually strong carbon-to-fluorine bonds” in these compounds make them resistant to natural decomposition. Yujie Men’s team at UCR recently found two species of bacteria, Desulfovibrio aminophilus and Sporomusa sphaeroides, that know how to break those bonds.
“What we discovered is that bacteria can do carbon-chlorine bond cleavage first, generating unstable intermediates,” Men said.
“And then those unstable intermediates undergo spontaneous defluorination, which is the cleavage of the carbon-fluorine bond.”
The team believes that providing these naturally occurring bacteria with nutrients like methanol in groundwater could increase their numbers. If they are not present, contaminated water could be inoculated with the bacteria. Why try to imitate their chemistry prowess when they are already at work doing what is needed? Just pamper them and PFAS can disappear.
The UCR team published their award-winning findings in Nature Water, but the bacteria are the deserving ones for a prize. This discovery adds to other abilities of bacteria to degrade pollution:
Microbes have long been used for biological cleanup of oil spills and other industrial pollutants, including the industrial solvent trichloroethylene or TCE, which Men has studied.
But what’s known about using microorganisms to clean up PFAS is still in its infancy, Men said. Her discovery shows great promise because biological treatments, if effective pollutant-eating microbes are available, are generally less costly and more environmentally friendly than chemical treatments. Pollutant-eating microbes can also be injected into difficult-to-reach locations underground.
While not an excuse to pollute, the findings give hope for cleaning our messes with gifted microbes.
Proficient Sorters
Some of the rare earth elements (REE) that are high in demand these days are difficult to separate. Again, a gifted bacterium is able to sort them better than humans can, announced researchers at Penn State. A protein in a bacterium may help pave the way for “green tech” with less cost.
Rare earth elements, like neodymium and dysprosium, are a critical component to almost all modern technologies, from smartphones to hard drives, but they are notoriously hard to separate from the Earth’s crust and from one another.
Penn State scientists have discovered a new mechanism by which bacteria can select between different rare earth elements, using the ability of a bacterial protein to bind to another unit of itself, or “dimerize,” when it is bound to certain rare earths, but prefer to remain a single unit, or “monomer,” when bound to others.
Instead of requiring toxic chemicals to do the separation, bacteria equipped with the LanM protein may be able to do it cleanly and quickly. The news item says that this bacterium lives on buds of English oak trees. Its ability to discriminate similar elements is very precise:
“This was surprising because these metals are very similar in size,” Cotruvo said. “This protein has the ability to differentiate at a scale that is unimaginable to most of us — a few trillionths of a meter, a difference that is less than a tenth of the diameter of an atom.”
Nature has reported on Penn State’s welcome discovery.
Mercury Impacts Earth
Concerned about mercury in your tuna and other seafood? Bacteria are coming to the rescue here, too. Scientists at Oak Ridge National Laboratory warn of the dangers of methylated mercury:
Methylmercury is a neurotoxin that forms in nature when mercury interacts with certain microbes living in soil and waterways. It accumulates at varying levels in all fish — particularly large predatory fish such as tuna and swordfish — and, when consumed in large quantities, can potentially cause neurological damage and developmental disorders, especially in children.
While microbes are involved in the formation of the toxin, scientists at Oak Ridge have discovered two species of methanotrophic bacteria that can degrade it.
Bacteria called methanotrophs feed off methane gas and can either take up or break down methylmercury, or both. Methanotrophs are widespread in nature and exist near methane and air interfaces, and both methane and methylmercury are usually formed in similar anoxic, or oxygen-deficient, environments.
To single out how and which methanotrophs perform demethylation, the ORNL-led team — along with methanotroph experts from the University of Michigan and Iowa State University — investigated the behavior of many different methanotrophs and used sophisticated mass spectrometry to analyze methylmercury uptake and decomposition by these bacteria. They discovered that methanotrophs such as Methlyosinus trichosporium OB3b can take up and break down methylmercury, while others such as Methylococcus capsulatus Bath only take up methylmercury.
In either case, the bacteria’s interactions can lower mercury toxicity levels in water.
The work is published in the open-access journal Science Advances by the AAAS. Perhaps safe tuna sandwiches are in our future, thanks to microbes.
Gut Helpers
A health partner inside our GI tract that many of us never heard of is named Akkermansia muciniphila. After enjoying a tuna sandwich, we depend on this little bacterium that lives inside us to avoid metabolid disorders. Here’s what it does for us, according to Phys.org’s report on findings at Duke University:
A. muciniphila can make up as much as 3 to 5% of the biota found in stool. It is present in wild animals, and its abundance in humans seems critical for healthy physiological functions, as abnormal levels are associated with immune disorders, pregnancy complications, cancer, neurological disorders and every kind of metabolic disease.
This gut germ helps regulate lipid biosynthesis and cholesterol levels. Would evolution generate as many redundant machines as this bacterium possesses?
A. muciniphila is known to use mucins as its preferred nutrient source. Mucins are large, highly glycosylated proteins that comprise the bulk of the intestinal mucus lining. The study found that, despite having the capability to produce a wide range of glycoside hydrolase enzymes, estimated to be around 60, only a few are needed to degrade intestinal mucins. This redundancy means that even if there were a mutation in one or most of these genes, the organism would still have the ability to survive.
Learn more about this essential microbe in Nature Microbiology.
Ocean Fertilizer
Another microbe — this one a cyanobacterium — performs a vital function for life in the seas. New Scientist describes how it changes its behavior depending on light levels.
These bacteria don’t just provide food for other organisms, they also turn nitrogen from the atmosphere into chemicals that other photosynthetic organisms can use. They fertilise vast areas of the ocean that would otherwise be too poor in nutrients for anything to grow, says [Ulrike] Pfreundt.
“It’s the living fertiliser for the oceans, essentially,” she says. “They provide a very large part of the nitrogen that is fixed in the ocean, and a whole lot of other organisms that sequester CO2 depend on this nitrogen.”
Our world could not function without microbes such as these, and uncountable numbers of additional species remain to be discovered. They are far from being mere primitive steppingstones to complex life. Without their engineering prowess to degrade harmful substances and provide nutrients for others, large organisms — animals and plants — could not exist. This elevates the evidence for intelligent design beyond cells and individuals to the entire biosphere.
Subscribe to:
Posts (Atom)