The second example of “devolution” in the article (the gut microbiome) has nothing to do with Behe’s thesis - it’s just documenting the nearly neutral theory of molecular evolution. It has nothing to do with adaptive mutations being “damaging”, it’s about most fitness-affecting mutations being non-adaptive! The quote even says that these non-adaptive mutations are purified in the long run, so it has little to do with long-term evolution.
The EN article quotes this part of the primer (not the original paper):
The observed patterns of between-host polymorphism reject the predictions of a simple neutral model of molecular evolution for several human gut bacteria. Synonymous site polymorphism (i.e., that does not lead to changes in the protein sequence) exhibits a variance clearly inconsistent with a model, in which neutral mutations arise in each host and a single lineage transmits between hosts. However, the pattern of polymorphism at synonymous and nonsynonymous sites is consistent with the slightly deleterious theory of molecular evolution [16], in which widespread purifying selection may keep a microbial ecosystem functional, at long time scales, for all hosts. Much of the variation observed can be explained by postulating the recurrence of a high fraction (90%) of mutations whose effects decrease fitness by a very modest amount (approximately 0.01%) but still strong enough to be purified in the long run.
But for some reason leaves off the very next paragraph, when Gordo begins to talk about adaptive mutations. Surely this is the part that might actually be relevant to Behe’s thesis?
When looking for signs of evolution (identity by descent with modification) within hosts, significant changes in SNV frequency could be detected on a time scale of six months (occurring in 12% of the time comparisons). This was possible even under the strong criteria imposed for low false-positive rates (frequency changes above 60%), which can greatly limit power to detect true events that may occur but remain undetected with this type of data. Of the identified events, approximately three-fourths involved a handful of SNVs rising to high frequency on a time scale of hundreds of generations. Such an observation is highly unlikely under neutral evolution (in which mutations would take a much longer time to change in frequency) but fully consistent with natural selection increasing the frequency of mutation and/or recombination created alleles having fitness effects of a few percent. The remaining one-fourth of the detected changes involved thousands of SNVs, compatible with the replacement of a dominant strain by a newcomer invader strain or with a rapid spread of another resident strain, which was colonizing that host at low frequency [14]. Furthermore, albeit under the strong filtering criteria imposed to avoid false negatives and/or positives, gene content differences could also be inferred. These involved gene losses (caused by mutation [deletions] or recombination) and gene gains, potentially recombination derived, which tended to change the accessory (noncore) genome.
Neither this primer that EN article quotes nor the original paper provide any evidence in favour of Behe’s thesis. The paper doesn’t do any kind of characterisation of the adaptive (or non-adaptive) mutations to see if they’re “damaging” or not.
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The 3rd example in the EN article (staying afloat) is even worse.
It quotes this press release about this paper.
The study looked at how robust protein interaction networks (interactomes) were to breakdown.
However, the subject of the paper is completely irrelevant, because the only point the EN author seizes on is a throwaway line from the press release about one way the breakdown of networks could happen: mutations.
Hold the presses! Mutations can break down networks of interactions! Wait, what does this have to do with Behe’s thesis again? Absolutely nothing. The EN article’s takeaway is simply:
Mutations do not construct new complex machines. This study says that they “gum up the works.”
The original paper is interesting though - worth a read.
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I also took a look at the 6 “short stories” mentioned at the end of the article:
1.
A paper in PNAS by Milner et al. shows that fungi can gain new functions! Yes, but the method is by horizontal gene transfer (HGT) — i.e., by borrowing existing genes. Scientists found that fungi can gain transporter-encoded genes by HGT, giving them a “distinct competitive advantage in a given environment,” they say. “This has wide implications for understanding how acquisition of single genes by HGT can drastically influence the environments fungi can colonize.” How many other claimed instances of gain-of-function mutations are really cases of HGT?
It’s a paper about beneficial fitness effects of HGT in fungi. How is this supposed to support Behe’s thesis that beneficial “non-damaging” mutations are rare? The last sentence reads as though the paper investigated cases of fitness increase that they presumed to represent a gain-of-function mutation but then were surprised to discover that they were actually HGT after all, but that isn’t what happened. The authors set out to identify cases of HGT and then examine their fitness effects.
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2.
Darwin is devolving in beehives. Here is the honeybee version of the children’s story, “The Town Mouse and the Country Mouse.” Phys.org says that the “waggle dance” method of communication is disappearing in urban settings. “One possible reason may be human-induced habitat change,” which led to the loss of this complex, informative behavior.
Oh finally, an actual case of “loss”. At least, that’s what the EN article’s phrasing and chopped-up quotes would have you believe. In fact, if you actually read the Phys article and the original paper it turns out there’s no mention of the “waggle dance” behaviour disappearing in urban settings. The paper is basically about the effectiveness of the waggle dance in different circumstances. Through experiments, they found that the bees were able to learn whether or not it was worth their time to pay attention to the waggle dance or just go off and find food on their own. They found that in “disoriented” experimental conditions (where the dance was meaningless), the bees learned after a few days to not bother paying attention because it was a waste of time. The authors relate these experimental results to real environments, and conclude that in some environments, at some times, the waggle dance might not improve foraging success. They say:
”If there is no benefit of dance communication in temperate climates, then why do bees dance? First, the dance might still be beneficial to foraging success in our study area during other time periods, e.g., in spring. Bee colonies may gain weight during only a few weeks per year. For this reason, it is critically important that the colony can exploit the high-quality resources available while there are good foraging conditions; the dance is likely to play an important role in maximizing foraging efficiency during such periods. Second, encoded spatial information is only one part of the dance. For example, forage odor plays an important role in honeybee foraging, and incoming dancers will distribute this information to followers during their dance displays ( 19 , 28 , 36 ). Dancers can also reactivate foraging at a patch by stimulating experienced foragers to revisit foraging sites ( 8 ). Thus, while the spatial information contained in the dance will likely have a fluctuating value over the seasons, the other cues may mean that dancing remains an important feature of the honeybee’s foraging success.”
In other words, there’s no reason to think that the waggle dance behaviour is “disappearing” anywhere. Even if it was, what do you expect? If the behaviour provides no fitness advantage, why shouldn’t it be lost? Is that how low the bar for Behe’s “devolution” thesis is? If a bird evolves a long beak to get at nectar in deep flowers, then later the deep flowers die out and are replaced by shallow flowers, would Behe cry “devolution!” if the birds evolved shorter beaks again?
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3.
Another Phys.org article says that antibiotic resistance genes “spread faster than so far thought.” The reason? It’s not the emergence of novel genes by mutation. Instead, “resistance genes hop around the genome.” Methods of gene sharing include viruses, phages, and transposons. An international team was surprised to find that “mobile genetic elements induce a fast distribution of resistance genes among genomes of different organisms.” One said, “The finding that resistance is also extensively transferred between bacteria without the involvement of plasmids is really quite surprising.”
Again, nothing to do with Behe’s thesis. Observing instances of HGT doesn’t mean that adaptive gain-of-function mutations are rare. I’ll add that from reading this paragraph from EN, I got the impression that the study in question represented some kind of huge, landmark study on the spread of antibiotic resistance from a large number of cases. In fact, it’s a quite small study, exposing fish to an antibiotic for a month and then looking at the gut microbiome for how the resistance genes spread. Also, contrary to what the EN authors writes, the paper does mention that several of the horizontally-transferred genes were mutated to confer resistance.
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4.
Scientists found a plant genome with “among the most GC-biased genomes observed to date.” The parasitic plant uses only six amino acids, and is 95 percent composed of AT base pairs. “Darwin help us!” exclaims the exasperated author David Roy Smith in Current Biology . Apparently these two parasitic plants have forsaken richer genomes because they are able to get by with less.
Several issues here. For a start it should be made clear that David Roy Smith is the author of the Current Biology article commenting on the original study in PNAS, he’s not the author of the study itself. Second, look at how the EN author managed to twist his words. In the comment piece, Smith says:
”I thought I had seen it all. However, the recent sequencing and characterization of two plastid DNAs (ptDNAs) from the holoparasitic plant genus Balanophora (Figure 1) has proved me wrong and raised the bar of what defines an extreme genome [1]. With AT compositions of 88.4% and 87.8%, the B. reflexa and B. laxiflora plastomes have a smaller proportion of GC base pairs than any other ptDNA explored to date. Even more remarkable, the AT bias is most prominent in the true heart and soul of these genomes: the protein-coding genes. It stands to reason that coding DNA should contain at least some guanine and cytosine in order to encode the correct cohort of amino acids needed for making functional proteins. I guess the Balanophora ptDNAs did not get this memo. Darwin help us, the ycf2 gene from both species is 98% AT! Or, put differently: across the 750 nt that make up this plastid gene, there are fewer than eighteen sites containing a G or C.”
Ok, that’s the exclamation in context, does Smith sound in any way “exasperated” there? He’s excited, for goodness’ sake, not irritated!
The EN author says “the parasitic plant uses only 6 amino acids, and is 95 percent composed of AT base pairs.” This is just a basic failure of reading comprehension. The paper isn’t about the plant’s whole genome, it’s specifically talking about the plastid DNA. The original paper and Smith’s comment piece both make it clear that about 80% (not 100%) of the proteins encoded in the plastids consist of only 6 different amino acids, and that “several genes” in the plastid have an AT content in excess of 95%, not all of the genes or the entire plastid genome.
All these errors aside, does this study really support Behe’s thesis? I suppose it’s a case of adaptation via loss, so perhaps it does, but then again it’s also exactly what is expected by natural evolution. Parasitic organisms becoming more streamlined has been known about forever, this case is just an extreme example.
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Let’s all evolve like the birds evolve. How do birds adapt their songs? With “preexisting genetic variation.” Lai et al., writing in PNAS , seemed to want to hear their favorite Darwin tune, but found that parrotbills in Taiwan select “standing genetic variation” instead of de novo mutations. They found that “the evolutionary potential of a population depends significantly on its preexisting genetic diversity.” Selection of existing genetic variation is likely to swamp new beneficial mutations, because “ a high level of standing variation may allow a faster response to environmental changes than waiting for appropriate mutations to arise. ” Understandably so.
What…? Does the author of this EN article think that all/most adaptation should occur via mutations that appear de novo after the selection pressure appears? It’s completely uncontroversial that standing genetic variation is a huge source of variation for natural selection to act upon. Also, where does the author think this standing variation originally comes from if not mutations? This is baffling, and again has nothing to do with Behe’s thesis.
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Are humans evolving new beneficial mutations? Analysis of the human genome at the University of Barcelona identified 2,859 genes that apparently have been under selective pressure. Further reading shows that some of these result from “ hybridisation of the human species with the Neanderthals and other hominid species,” which implies sharing of existing genetic information. Other genetic changes aiding survival in certain environments, such as for lactose tolerance or ability to endure high altitudes (hypoxia), may result from relaxation or breaking of controls of existing genes. Overall, the research is revealing “how the introgression of archaic genomes have modelled our current genomes.”
Another completely irrelevant study to any of Behe’s ideas. The EN author doesn’t even attempt to write a “gotcha” sentence or two about these results. Some beneficial variants came from introgression, yes, the point being…?
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Conclusion
Honestly this is one of the worst EN articles I’ve ever read. Of the 9 studies they cited that supposedly supported Behe’s “devolution” thesis, literally none of them came close to doing so.