u/jnpha

Published today in Molecular Biology and Evolution.

It caught my eye right away as I've been (on and off) reading Homology, Genes, and Evolutionary Innovation (GP Wagner, 2014).

An example of modularity is our digit 1 (the thumb). Digits 2 to 5 are correlated, developmentally and evolutionarily, whereas digit 1 has become its own module in primates, facilitating uncorrelated adaptation:

> Specifically, digit 1, the thumb, expresses only two Hox genes, HoxA13 and HoxD13, whereas digits 2 to 5 additionally express HoxD12 to HoxD9. Reno and colleagues showed that the morphological correlations among digits 2 to 5 were much higher than the correlations between digit 1 and all other digits both in terms of population variation and evolutionary differences. In primates, the thumb shows more independent evolutionary change relative to the other four digits than each of digits 2 to 5 relative to each other. Hence, Reno et al. identified two variational modules in the primate hand: digit 1 and one module comprising digits 2 to 5.
(GP Wagner, 2014)

How modularity comes about is interesting; for example it can be a consequence of selection on robustness: Robustness (evolution) - Wikipedia. This is something Andreas Wagner's (another Wagner) lab has been working on, and on my reading list is his Arrival of the Fittest (A Wagner, 2014).
You can find his lecture on a related topic, given at the Royal Institution, here: https://www.youtube.com/watch?v=aD4HUGVN6Ko

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Back to today's paper:

Structured abstract:

Background

> Understanding how the myriad molecular impacts of mutation percolate to influence higher-order traits and ultimately fitness requires compressing a many-to-many mapping into something tractable. Decades of theoretical work suggest this may be possible because biological systems are modular: effects of perturbation are often funneled through particular pathways or subsystems rather than propagating freely through the organism. Yet, few empirical systems have been able to demonstrate such modularity at scale.

Results

> Here, we show that, even across 774 diverse yeast lineages, fitness variation across 12 drug environments is organized by a strikingly low-dimensional structure defined by only a few inferred phenotypic axes that capture the main patterns of variation. Lineages drawn from multiple evolutionary histories reveal more of these phenotypic axes than those derived from a single selection pressure. Consistent with many of these lineages having evolved under strong selection pressure, their mutations often exhibit broad pleiotropy, affecting nearly all inferred phenotypic axes.
However, fitness in any given drug depends on a much sparser subset of the phenotypic modules these axes reflect. By compressing many-to-many relationships, this low-dimensional framework exposes the modular phenotypic space, as well as the context-dependent contribution of each phenotypic module to fitness that can constrain the pleiotropic effects of adaptive mutations. It also highlights that the apparent complexity of genotype–phenotype–fitness maps depends not only on environmental context but also on the diversity of mutations through which they are observed, laying the groundwork for identifying the key phenotypic modules that matter for fitness.

and from the discussion:

> Our results echo ideas from the omnigenic perspective on complex traits, which holds that mutations in many genes can shape trait variation through dense regulatory networks (Boyle et al. 2017; Liu et al. 2019). In our case, mutational effects did not scatter unpredictably but instead collapsed onto a small set of shared axes. A recent quantitative omnigenic model formalized this principle, showing that network-level complexity can be summarized in low-dimensional, interpretable structures (Ružičková et al. 2024). The key difference is that while the quantitative omnigenic framework is a bottom-up approach deriving axes from regulatory network topology, our top-down SVD approach infers them from observed fitness patterns alone. Yet, both converge on the idea that molecular complexity funnels through a limited set of modules that enable prediction.

(all emphasis mine)

 

• Mohammad Hossein Donyavi, Reza Ghelich, Kara Schmidlin, Grant Kinsler, Kerry Geiler-Samerotte
  Evolutionary adaptation proceeds through a small number of phenotypic modules
  Molecular Biology and Evolution, Volume 43, Issue 8, August 2026, msag183, https://doi.org/10.1093/molbev/msag183

Published today in Molecular Biology and Evolution:

Structured abstract:

Background

> The vast majority of plants form mycorrhizal symbioses. The ecological importance of these mutualistic interactions has sparked interest in their long evolutionary history. By examining interaction networks and phylogenetic trees, several studies have suggested that plants codiversify with their associated mycorrhizal fungi. However, recent research has demonstrated that phylogenetic congruence (interpreted as codiversification when divergence times match) is often conflated with another pattern called cophylogenetic signal (i.e., closely related plants interacting with closely related fungi and vice versa), which may arise from different biological processes.

Methods and results

> We performed cophylogenetic analyses on 29 diverse mycorrhizal networks to reevaluate the evidence for codiversification in mycorrhizal symbioses. We found significant cophylogenetic signal but no phylogenetic congruence: closely related plants often interact with closely related fungi, but their phylogenies do not match. Instead of codiversification, this finding is consistent with trait matching between plants and mycorrhizal fungi, where compatible, evolutionarily conserved plant and fungal traits govern their interactions.

Discussion

> Our work highlights the importance of appropriately interpreting the cophylogenetic methods used to study the macroevolution of plants and their mycorrhizal fungi. It suggests that previous evidence of codiversification in mycorrhizal symbioses actually detected cophylogenetic signal, since across the multiple and diverse networks analyzed here, there is no evidence that codiversification occurred during the evolution of mycorrhizal symbioses.

 

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• Fantine Bodin, Hélène Morlon, Benoît Perez-Lamarque
  Questioning the Evidence for Host-Symbiont Codiversification in Mycorrhizal Symbioses
  Molecular Biology and Evolution, 2026;, msag207, https://doi.org/10.1093/molbev/msag207

Caption:

> HRF [hemiplasy risk factors] values are highest near the origin of Neoaves.

Explanation:

> Hemiplasy — which arises due to discordance between gene trees and species trees — can cause traits to appear convergent despite a single origin. New evidence suggests it is widespread in the bird tree of life, with important implications for identifying genes underlying differences among species and for accurately inferring evolutionary history. ref

From the paper:

> We show extremely high hemiplasy risk factors^(19) that map to branches near the origin of Neoaves, suggesting that many instances of apparent morphological convergence among major neoavian lineages, unless associated with clear selective drivers, are better interpreted as a result of high levels of morphological incomplete lineage sorting during the clade’s rapid early Cenozoic radiation.

The paper:

• Somogyi, Stanley, et al. "Hemiplasy helps explain high rates of apparent morphological convergence in neoavian birds." Current Biology 36.9 (2026): 2424-2433. https://doi.org/10.1016/j.cub.2026.03.050

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An example that is closer to home is how 23% of our genes are closer to gorillas than chimpanzees (Ebersberger et al 2007). This is as predicted from gene tree discordance (e.g. Degnan & Rosenberg 2006) and confirms that chimps are our closest cousins; for a video explainer by Dr. Zach Hancock: Phylogenetic Discordance Supports Common Ancestry - YouTube.

u/hUserName's post (Is it normal for fuel to be coming out of wings?) reminded me that I wanted to share this

Source:
The Aviation Show - The Original B-47 Stratojet Pilot Familiarisation Film (1952) https://www.youtube.com/watch?v=1Za8Z3-aEyo

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Was this solved by the fuel atomizers?

"Where are all the designs?" is a damning observation against creationism^(1), as well as some food for thought. It's an old observation, e.g. this paragraph in Darwin's Origin (1st ed.), which has stuck with me, especially the part I put in bold:

> ... We meet with this admission in the writings of almost every experienced naturalist^(2); or, as Milne Edwards^(3) has well expressed it^(4), nature is prodigal in variety, but stingy in innovation. Why, on the theory of Creation, should this be so? Why should all the parts and organs of many independent beings, each supposed to have been separately created for its proper place in nature, be so invariably linked together by graduated steps? Why should not Nature have taken a leap from structure to structure? On the theory of natural selection, we can clearly understand why she should not; for natural selection can act only by taking advantage of slight successive variations; she can never take a leap, but must advance by the shortest and slowest steps [...] why this should be a law of nature if each species has been independently created, no man can explain.

 

Example
Most creationists I've seen think bird wings are an innovation, but they are a variation of forelimbs: the same body plan of bats, cows, us, mice, etc.; in this case Tetrapoda is prodigal in variety, not in innovation.
Nor does gradualism mean constant-speedism, anticipating the regurgitation of the 1980s creationist twisting of Gould's work, a red herring while the observation remains.

My footnotes:
(1) beating a should-be dead horse but it keeps popping up here: the term since the 60s is not a reference to theism
(2) old-timey word for scientist - given the irrational creationist fear of methodological naturalism, sadly, this needs pointing out
(3) French zoologist (1800-1885)
(4) I did change one word that is often misunderstood for a slur

 

And the same thing is also present in the percolation of protein space, e.g. this 2026 study: Maynard Smith’s analogy, realized: Common ancestry constrains evolutionary percolation through protein space | PNAS.

 

In short:
Creationism cannot explain the limited innovation and high variety, which is present at all levels, from body plans to proteins.
Science, on the other hand, didn't ignore this observation, and as the linked research shows, it is testable even at the sequence space level.

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And I cannot not mention ID: ID of course pretends to answer this by appealing to big scary numbers based on backwards probabilities, and then they get cooked by actual research, which, ofc, they continue to ignore; e.g.: Frumkin et al. (2025) demonstrate the "surprising ease with which functional genes can emerge" from random sequences : DebateEvolution.

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edited to add the example

Published today:

• Chinese Academy of Sciences press release:
  Sticky alpine flower confirms Darwin's 150-year-old carnivorous plant prediction

• Paper:
  Zhang, XJ., Deng, T., Lin, N. et al.
  Identification of carnivory in the flowering plant Saxifraga via multidisciplinary evidence.
  Nat Commun 17, 7557 (2026). https://doi.org/10.1038/s41467-026-75288-y

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Excerpts from the paper:

> ... Inspired by his work on carnivory in Drosera, Darwin (1875) proposed that two Saxifraga species (S. rotundifolia and S. umbrosa) might similarly exhibit carnivorous behavior. Darwin regarded these two species as representing one of the most intriguing cases among plants with glandular hairs^(2). Although Darwin attempted to test this hypothesis through feeding experiments, these early attempts did not yield conclusive results^(2). > > ... To investigate the potential status of S. candelabrum as a carnivorous plant (Fig. 1), we test the four key criteria required to confirm carnivory (prey attraction, capture, digestion, and nutrient uptake). Specifically, we address the following questions: (1) Does the plant actively attract and capture insect prey? (2) Can it directly digest prey and absorb derived nutrients? (3) Does it exhibit convergent genomic signatures with other carnivorous lineages^(20)? > > ... Our findings provide definitive evidence of carnivory in Saxifraga, addressing Charles Darwin’s long-standing hypothesis that some Saxifraga species may be capable of carnivory, and further suggest that carnivory may be more widespread among angiosperms than previously recognized.

 

Basically the title question, but I'll explain where this question is coming from.

YECs are inculcated and primed from a young age that evolution (and "materialism" and "secular science") leads to a bleak world view, leads to sin, etc. etc. (the stuff we see here and elsewhere). Ofc what concerns us here is the science - I'll give two examples before getting into where this is coming from:

When we first learn the science behind how a dropped bullet hits the ground at the same time as a bullet that was fired horizontally, something wonderful clicks! you can't arrive at that using common sense (common sense is actually proposed to have been behind the late arrival of the scientific revolution).
Another example is how it wasn't surprising (to the experts) when it was discovered that we, bonobos, and chimps, are all equally related to gorillas (Gutsick Gibbon's recent video on that - the fact amazes me Every Single Time I hear it). This is a brute fact regardless of what comparative genomics method is used, and applies whatever the sister taxa may turn out to be, and the science behind it is also impenetrable - and awesome ("common sense" would say chimps are closer to gorillas).

Ofc both examples are neither intelligible nor amazing to someone who still holds to the Aristotelian-era common sense notions of impetus and scala naturae, respectively, and that's the point.

 

Now, the reason behind this post: a couple of days ago I remembered an interview I came across when I was looking into the details of the Dover trial. So a quick background: Kenneth R. Miller is a scientist (who happens to be Christian) who was one of the expert witnesses for the plaintiffs (the agrieved parents) during the 2005 Dover trial.
He's also known for his science public outreach, and e.g. this really cool lecture from 2006 at Case Western Reserve University, The Collapse of Intelligent Design, where he showcased the stupidity and dishonestly of the ID movement (must watch for any newcomer here imo).

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Side note: re that video title, while we have the benefit of hindsight of 20 years, Miller should have heeded Hilaire Belloc (1929):

> The good fortunes of stupidity are incalculable. One can never tell what sudden resurrections ignorance and fatuity may not have.

(thank you u/LightningController for sharing this quotation!)

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Back to said interview; here's that part of it:

> ... with the passing of Steve Gould - and Steve unfortunately died in '02 - I'd have to say that I think Richard Dawkins is the clearest and most lucid writer on evolutionary theory that's alive on the planet today. His book The Selfish Gene, I think, is a classic of explaining behavioral biology. His book called Unweaving the Rainbow is a marvelous long essay on how science doesn't diminish our appreciation for the beauty of nature, it enhances it, and he writes brilliantly and well.

Remember, this is a Christian, talking about YEC's and ID's goliath^([*]). Continuing:

 

> ... Now, you know, I'm not trying to be flip - some of my best friends are atheists. Um, in science, that's not a big deal, and we work in science, we don't know what anybody else's religious point of view is because science is science, and we get along just fine.

(my emphasis)
Then he talks about Dawkins' feedback on a new book of his, where he found an error, and:

 

> So four or five days later, he's on a trans-US tour. I get an email from Richard. He's now in Los Angeles and he goes, "I have now read the rest of your book. Needless to say, I disagree with everything in Chapter 6" ... But then he said - and this is one of the reasons I decided to respect the guy - he says, "You try to explain the Multiverse hypothesis of Barrow and Tipler. You misunderstand it, and the reason I know you misunderstand it is the way you interpret it is the same way that I, Dawkins, first understood it, and I was corrected at a scientific conference by John Barrow himself." He then gave me the reference to the article in the journal. I looked it up, and by God, he was absolutely right. And everything since the, every printing since the first printing in hardcover has had the correct explanation. So if you buy a paperback book, it's fine. > > What I appreciated about Dawkins was, I said a lot of bad things in that book that were critical of him. What he could have said is, he could have written a review saying, "Look what an idiot this Miller guy is. He doesn't even understand the Barrow and Tipler hypothesis, therefore why should you believe anything else to be said?" And instead, he did sort of the gentlemanly thing, which is, "You made the same mistake I did. Let's correct that mistake, and then let's argue about things that really matter."

 

Isn't that wonderful. Science doesn't diminish our appreciation for the beauty of nature. Science is science. And scientists who happen to be atheists, like those who happen to be theists, care only about the facts.

The other extreme ofc are the cartoon characters we see here: the YEC and/or ID reality deniers (and their various propaganda outlets) - who think an inference from the unknown, or elbow-greasing (some of) the data into the "revealed" model, is doing science. Now, given that we necessarily counter using brute facts when we are dealing with that stupidity, I think this post might be a nice change of pace (also it's on-topic), and ofc the title question is open to all (not just former YECs).
(no, Robert, there are no ad hominems in this entire paragraph)

 

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* Back to that "goliath" asterisk above; here's ID founder Phillip Johnson in 2001:

> It isn’t worth my while to debate every ambitious Darwinist who wants to try his hand at ridiculing the opposition, so my general policy is that Darwinists have to put a significant figure at risk before I will agree to a debate. That means specifically Dawkins or Gould, or someone of like stature and public visibility.

Anyone here remember the "Where are the Dawkinses?" idiot? They really are living in cartoon land. (that's still a no, Robert)

/s for the title

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If I had a nickel...

A Telegraph (which is was generally reliable) piece was published today, was shared on r/ evo, and its OP took it down after 1 comment; the piece: Why Darwin’s discredited rival may be proven right 200 years later.

As a taste:

> Prof Edelaar also pointed to killer whale mothers that acquire the skill to hunt a different type of prey, such as seals instead of salmon, and claimed that this skill was then copied by their offspring.

You mean... learning???
What fucking year is this.

Sorry this was too funny not to share; also see: The Nobel Prize in Physiology or Medicine 1973 - Press release - NobelPrize.org.

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And since the propagandists repeat the same when it comes to their bogeyman the "modern synthesis" (a period in time), feel free to hit 'em with this next time you see them:

> ... Wright [one of the founders during the Modern Synthesis] was aware of this and argued that reaction norms enabled an uncoupling of the genotype from the phenotype ... It was Dobzhansky [one of the founders during the Modern Synthesis] who brought the reaction norm into the Modern Synthesis by arguing that the reaction norm was the focus of selection, leading to changes in relevant gene frequencies enabling particular developmental sensitivities and a range of response to become fixed in the population (Sarkar 1999). This view of reaction norms led to the more general concept of phenotypic plasticity which relies upon the genotype–phenotype distinction incorporating reaction norms and all kinds of “environmentally induced phenotypic variation” (Stearns 1989: 436).
doi:10.1007/978-3-031-22028-9_26

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Also see:

• Dr. Zach's post, Lamarckian evolution is (still) false : evolution

• And a new study I shared here that has achieved a "rare feat": The "It's epigenetics, not evolution" crowd : DebateEvolution

 

Over to you - again it was too funny not to share, and we're bound to hear about it soon (I called it last time around).

• Yamanouchi, Kei, Hinata Moriya, and Shin-ichi Yokobori.
  "Resurrecting tRNAs of the Last Universal Common Ancestor (Commonote) Toward Rebuilding the Ancient Translation System." Journal of Molecular Evolution (2026): 1-25.
  https://pubmed.ncbi.nlm.nih.gov/42423740/

> Ancestral sequence reconstruction (ASR) was used to study the evolution of the translational system by inferring tRNA sequences of the Last Archaeal Common Ancestor (LACA), the Last Bacterial Common Ancestor (LBCA), and the Last Universal Common Ancestor (LUCA), referred to as "Commonote" in our previous studies. A composite phylogenetic tree inferred from the reconstructed ancestral tRNA sequences revealed a topology distinct from those of previously inferred aminoacyl-tRNA synthetase (ARS) trees. This incongruence may reflect changes in tRNA structural features or distinct evolutionary pressures on tRNAs and ARSs, suggesting a more nuanced evolutionary history of the translation system, but it may also arise from methodological differences between studies. Phylogenetic analysis identified conserved identity elements, such as the discriminator base and anticodon, across tRNAs for different amino acids, supporting their status as ancestral features. Most LUCA tRNA species retain bacterial identity elements, potentially enabling their use in modern systems such as Escherichia coli, although exceptions, including tRNAGly and initiator tRNAMet, may present functional limitations. To evaluate the translational functionality of LUCA tRNAs and ancient codon-anticodon interactions, synthesized LUCA tRNAAla and tRNASer variants with anticodons decoding ACN codons were tested in an E. coli reconstituted in vitro translation system. These reconstructed tRNAs successfully decoded ACN codons, with tRNAAla variants exhibiting translation efficiencies comparable to those of native E. coli tRNAThr. Notably, decoding patterns differed from Crick's and extended wobble rules, as anticodons with various first-position bases recognized multiple third codon positions. This study offers new insights into the early evolution of the translation system and demonstrates the functional potential of ancestral tRNAs in contemporary contexts.

 

and

• Wehbi, Sawsan, et al.
  "Tryptophan became part of the universal genetic code post-LUCA." bioRxiv (2026): 2026-05.
  https://www.biorxiv.org/content/10.64898/2026.05.28.728509v3
  (preprint)

> We evaluate whether tryptophan (W), widely thought to be the last of the 20 canonical amino acids added to the genetic code, was already present in the Last Universal Common Ancestor (LUCA). We reconstruct the evolutionary history of tryptophanyl-tRNA synthetase (WRS), the enzyme that attaches W to its tRNA, and the related tyrosyl-tRNA synthetase (YRS). We identify and exclude sequences derived from ancient recombination between archaeal and bacterial YRSs. Diverse rooting methods, including a novel approach exploiting time non-reversible evolution, all place the root between bacterial and archaeal YRS rather than between YRS and WRS. This supports post-LUCA WRS origination in Archaea, followed by its horizontal transfer to Bacteria. However, ancestral sequence reconstruction suggests that Archaea were depleted for W while Bacteria were not, and enzymes essential for W biosynthesis emerged in Bacteria. This suggests that W usage originated in Bacteria, with later WRS emergence in Archaea allowing the archaeal genetic code to converge with the bacterial code. The universality of the genetic code is usually attributed to common descent from LUCA, but the final step making the code universal was instead achieved by horizontal gene transfer. This gives credence to similar mechanisms for earlier steps in genetic code evolution.

 

For a recent press release on this sort of research avenue:

• Researchers trace genetic code's origins to early protein structures

And a cool open-access easy to read review/beginner's guide:

• Barbieri, Marcello. "What is code biology?." Biosystems 164 (2018): 1-10.
  https://doi.org/10.1016/j.biosystems.2017.10.005

Published today in Cell, open access:

> Summary
Reproductive isolation within and between populations was conventionally thought to proceed gradually through many mutations of small phenotypic effect. Contrary to this view, recent theory predicts that large-effect mutations become plausible when populations are far from their phenotypic optimum. Changes in pollinator assemblages severely compromise the reproductive success of many angiosperms, creating conditions conducive to mutations of large phenotypic effects. Here, we explore the role of major-effect genes in the evolutionary shift from hawkmoth to bee pollination in Petunia. By modifying six genes in the ancestral hawkmoth-pollinated P. axillaris phenotype, we created a mimic of the bee-pollinated P. secreta flower that is indistinguishable from this naturally evolved species both in its visual appearance and in behavioral assays. This study uniquely identifies the complete set of genes explaining the shift between two species, providing rare and compelling evidence for speciation by large-effect mutations.
https://doi.org/10.1016/j.cub.2026.07.007

 

In journal club fashion, I have a sort of critical remark:

This part, "Changes in pollinator assemblages severely compromise the reproductive success of many angiosperms, creating conditions conducive to mutations of large phenotypic effects", is super cool! but I take minor issue with the wording of the summary/discussion.

While it is a major-effect, the authors themselves note that the "Expression specificity minimizes pleiotropy of large-effect speciation genes" (my emphasis). (Hence my clearer title, where I include the "low-pleiotropy".)

I'm fairly confident that big changes to phenotypes that are not heavily integrated (low pleiotropy) don't go against the mainstream view of gradualism. In fact, this can only be so if they are indeed low pleiotropy (this isn't a "hopeful monster"):

From a year ago which I shared here: New study: Evolution of Dosage-Sensitive Genes by Tissue-Restricted Expression Changes : evolution.

The title above is taken from the title of Dr. Dan's (u/DarwinZDF42) video from yesterday: https://www.youtube.com/watch?v=gnuhi-Te0ZI

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It's an absolute gem, and is only 10 minutes long. It addresses the creationists' PRATT (debunked online since at least 2004) about mitochondrial eve.

I went in expecting Dr. Zach's style of a whiteboard and math math, instead, it was an Excel sheet, and two operations: multiplication * and division /. That's it. And the imagined YEC timeline is cooked, using the paper that they themselves cite.

The reason I'm posting this, besides sharing the fun video, is Dr. Dan also mentioned briefly what the impact of selection would be, and this got me thinking...
The YEC model for denying reality - like Discotute's latest movie, which doesn't mention the word "suffering" at all - doesn't take into account the impact of mutations. If the mutation hits the "wrong" spot, how would that change reach fixation? How?!!1!

That's it. Just sharing yet another self-contradiction.

Tour also complains that scientists invariably have to cheat 😱 - because the results scare him and so he pretends not to know how chemistry is done.

 

Ready for an excerpt from Discotute's cinematic production, The Story of Everything (2026) ⭐5.5/10 (https://www.imdb.com/title/tt13374694/) ?

> JAMES TOUR:
Since Kenyon announced his doubts [my emphasis, point later], there have been many other attempts to simulate how the molecular compounds necessary for life, like proteins and DNA, or even simpler chemical building blocks of those compounds, might have evolved under realistic prebiotic conditions on the early Earth. But those laboratory simulations invariably require a cheat. Human interference. When you do organic synthesis, when you make a compound, you need to generally start with pure compounds because the impurities cause a lot of deleterious reactions to occur. Once you've made your compound, you've got to stop it at exactly the right time before it decomposes, more human interference. Now, what you have to do is you have to separate it from all the other compounds that formed. Separations are really hard, really hard. Huge human involvement. Now you have to identify it. You have to know what it is and characterize it in order to bring it on to the next step. How do you go on? And the poor early Earth was mindless. It didn't know what it was supposed to make. Molecules have never been known to move toward life. Never, ever, ever. Molecules don't evolve toward life. They don't. > > STEPHEN MEYER:
Attempts to simulate how life could have arisen from a prebiotic environment involve an element that never gets acknowledged. And that element is intelligence. > > JAMES TOUR:
We need to address more fundamental questions. What's the origin of the code?

 

To Tour's question, I say, read a book, or this: Answering Will Duffy's challenge to Richard Dawkins: the origin of the genetic code : DebateEvolution

 

And in other You Won't Believe! News: the "docu" also has all your favorite totally-science-and-not-apologetics^(/s) PRATT:

From if there's a garden then where's the gardner (the irony of the example), to Penrose's 1 in a 10^10^123 spherical cow (corrected by https://arxiv.org/abs/0907.0659), to quote mining Dawkins (the fuller context), and of course, the running theme being that we have "two stories" (throwback to 1981),
and on that note, which is on-topic for this sub, back to my earlier bold emphasis:

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The bread and butter of the creationism/ID anti-science propaganda machine is taking academic discussions out of context, and using that to present a false dichotomy - they've been doing that since the 1880s, and here's a 2025 example that I reviewed here.

So here's an analogy:
Long after heliocentrism had been settled, precise measurements of Mercury's orbit were made, and they didn't match the expectation, and it was a whole episode of academic disputes. But if a propagandist had then come along and said, "A-ha! they can't agree, therefore geocentrism because my presuppositions", here the regular debateevo "skeptic" would come along and say, "See! there is disagreement, so it's 50-50, and I'll go with my geocentric gut because my presuppositions".

Am I taking the analogy too far, straw manning? I wish. And it's called false balance.
The "skeptic" here now will pause, think, and say, "But see, general relativity solved that one!" (as if this counters the false balance), but if GR was the topic, they'd say, "They still haven't quantized gravity, therefore fine-tuning something something" (n.b. cooked by https://arxiv.org/abs/1902.03928).

It's motivated thinking all the way down, and the propagandist and the skeptic are each bamboozling themselves - a match made in heaven.

 

Published 2 days ago, in press:

> Biologists have long sought to understand the forces driving biological speciation. Contrasts in dispersal ability (e.g., migration) are hypothesised to influence rates of lineage diversification. However, past inferences of migration-diversification relationships have been contradictory, suggesting the need for further investigation and more nuanced explanations. Here we test for a relationship between diadromy (marine-freshwater migration) and diversification in salmonids, a dominant group of fishes native across the temperate Northern Hemisphere. We reconstruct a molecular phylogeny comprising 140 species and apply State-dependent Speciation Extinction models to quantify diversification. Diversification rates are higher in non-diadromous relative to diadromous salmonid lineages, echoing the findings of a recent study of homologous southern temperate freshwater fishes, but conflicting with global studies incorporating tropical lineages. Climate appears to be a key factor explaining diadromy-diversification relationships, with the negative relationship observed in temperate lineages likely reflecting increased isolation and speciation of non-diadromous lineages following recolonisation of glacially perturbed habitats. In contrast, the positive diadromy-diversification relationships observed in studies spanning tropical fishes may reflect the role of diadromy in facilitating colonisation of stable, low-competition habitats.

 

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• Christopher P Burridge, Luke Simpson, Mark V H Wilson, Jonathan M Waters
  Non-migratory lineages experience higher diversification rates: global evidence from salmonid fishes, Evolution, 2026;, qpag131, https://doi.org/10.1093/evolut/qpag131

Excerpt:

> Importantly, they also found that promoters, which control transcription of adjacent genes, can act as distal enhancers when placed in a new genomic location (Fig. 1b). In other words, the specific role of any regulatory element depends highly on its genomic context. To Lowe, this fluidity between promoters and enhancers was the biggest surprise from their work. He hypothesizes that “promoters and enhancers are not distinct functional categories, and not many mutations are needed to convert a DNA sequence between acting as proximal or distal regulators of transcription.”

 

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Highlight article:

- Pedro Andrade, Highlight: Segmental duplications at the center of regulatory innovation, Molecular Biology and Evolution, Volume 43, Issue 7, July 2026, msag163, https://doi.org/10.1093/molbev/msag163

> Our findings challenge the view that human geometric reasoning is categorically distinct from that of other primates (1, 3, 4). Instead of a categorical divide, we find that monkeys and humans share a common representational space, relying on perceptual codes with graded contributions from abstract or symbolic-like features. Consistent with prior work, adult humans showed the strongest symbolic effects during geometric reasoning. However, we reveal that humans, particularly preschool children, share a common architecture with nonhuman primates rather than categorically different representations. This is important because it suggests that the stronger symbolic representation in adult humans is acquired rather than inherent. Our findings identify rotation invariance as a key component of this abstraction, suggesting that what has been interpreted as uniquely human symbolic structure may instead reflect increasingly powerful orientation-independent representations.

• Press release:
  Children and monkeys share common understanding of geometry

• PNAS paper:
  J. Li, I. Boni, L.R. Sandwick, E.M. Sanford, C.M. DeLong, L. Wenjie, M.M. Henderson, S.T. Piantadosi, & J.F. Cantlon
  Continuity in geometric intuition between humans and monkeys
  Proc. Natl. Acad. Sci. U.S.A. 123 (30) e2532934123
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