u/jnpha

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Source (the spoiler tag is for those who want to quiz themselves!):
Race Highlights | >!2021 Hungarian!< Grand Prix - YouTube

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First image source: Matt from Melbourne, Australia, CC BY 2.0, via Wikimedia Commons

Published yesterday in PNAS:

Abstract

> ... [We] show that the toxins evolved through two distinct genetic paths. The factor X and factor V toxins evolved through the sequential de novo co-option of ancestral clotting factor proteins that entailed their heterotopic expression in the venom gland, the fixation of segmental duplications containing each locus, and subsequent gain-of-function mutations that rendered factor X and factor V constitutively active. In contrast, the phospholipase A2 and Kunitz-type toxins evolved by modifying the functions of neurotoxins that were part of the venom arsenal. > > Our findings support models in which innovative mutations in single-copy genes precede gene duplication in the evolution of novel proteins and offer a rare view into the genesis of a complex trait that has played a central role in a major adaptive radiation.

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On that last point - how innovative mutations preceded gene duplication - from the paper:

> In his landmark book, Ohno proposed that gene duplication was a necessary prerequisite for the origin of new protein functions because duplication would allow one copy to retain the ancestral function while the second copy could incorporate new functional mutations (neofunctionalization) (17). However, this classic model has been challenged on the theoretical grounds that if newly duplicated genes are selectively neutral, they must acquire new, innovative, and selectable mutations before acquiring inactivating mutations (nonsense mutations, frameshifts, and deletions) (66–68). It is now recognized that the latter is much more probable than the former. Therefore, it has been proposed that innovative mutations may occur initially in single-copy genes and impart some new function such that subsequent gene duplicates may then be positively selected for and fixed on the basis of the new function (68, 69). A variety of empirical studies have demonstrated innovative mutations occurring before gene duplication (70–73). Several observations here prompt us to postulate the relative order of major genetic events in the evolution of procoagulant venom toxins that bear on these general models of genetic innovation. > > [...] > > We suggest that the first genetic change in the ancestral liver-expressed, clotting factor gene was the gain of its heterotopic expression in venom gland tissue (co-option; Fig. 6, step i) (our line of reasoning also applies to venom factor V, discussed below). Two key pieces of evidence for this scenario are the low but significant RNA expression of the predominantly liver-expressed F10 orthologs in venom gland tissues and the presence of the corresponding hemostatic proteins in venom. If expression in the venom gland evolved after gene duplication, then one of two F10 genes (the liver-expressed gene) would not be expected to be transcriptionally active in venom gland tissue. The observed expression of the liver-expressed F10 paralog in the venom gland is consistent with the ancestral single-copy F10 gene evolving expression in the venom gland before gene duplication, then decaying to some degree in the liver-expressed paralog after duplication.

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Awesome detective work!
It made me wonder whether venom glands and livers are developmentally related during cellular differentiation.
From a quick visit to Google Scholar, I found a tentative answer:

> Cells that comprise complex tissues often express different sets of genes due to functional differentiation between cell types; such cellular heterogeneity is found ubiquitously across many tissue types (Heindl et al. 2015; Ben-Moshe and Itzkovitz 2019).
Single-Cell Heterogeneity in Snake Venom Expression Is Hardwired by Co-Option of Regulators from Progressively Activated Pathways | Genome Biology and Evolution | Oxford Academic

And the second citation is about livers, so they have that in common with venom glands!

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• J. van Thiel, N.L. Dowell, C.F. Smith, E.E. Sanchez, & S.B. Carroll
  The genomic origins and evolutionary path to a key innovation in the world’s most venomous snakes
  Proc. Natl. Acad. Sci. U.S.A. 123 (37) e2621054123
  https://doi.org/10.1073/pnas.2621054123 (2026)

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Published yesterday in PNAS:

Background

> Repeated divergence across contrasting habitats is widely used to infer natural selection and adaptation. Such comparative inferences, however, remain inherently correlative and capture only adaptation shared among populations from the same habitat type, thereby missing site-specific adaptation unique to individual populations. Field transplant experiments test adaptation directly by measuring fitness in nature but are typically limited to pairwise reciprocal exchanges between populations and therefore cannot distinguish between habitat-level and site-specific adaptation.

Methods

> Here, we extend the typical transplant framework to include multiple populations from both within and across habitat types, allowing fitness variation to be partitioned into shared habitat-level and unique site-specific components. We apply this framework to lake–stream stickleback, a classic system for studying adaptation via repeated divergence. Specifically, we transplanted laboratory-reared fish from a panmictic lake population and four independent stream populations across one lake and two stream sites.

Results

> Stream fish outperformed lake fish in streams and vice versa, demonstrating adaptive divergence across the lake–stream divide. However, at both stream sites, local stream fish also outperformed foreign stream fish. Strikingly, this site-specific advantage was twice as large as the advantage of shared stream adaptation reflected by the fitness benefit of foreign stream fish over foreign lake fish.

Discussion

> These results show that most fitness-relevant evolutionary variation in this system is unique to individual populations and therefore invisible to approaches that rely on repeated evolution to infer adaptation. More broadly, our work underscores the importance of ecological scale for understanding adaptation and evolutionary predictability.

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• M. Roesti, H. Roesti, H. Sudasinghe, N. Nesvadba, V. Saladin, & C.L. Peichel
  Disentangling unique site-specific and shared habitat-level adaptation in a classic system of repeated evolution
  Proc. Natl. Acad. Sci. U.S.A. 123 (36) e2612038123
  https://doi.org/10.1073/pnas.2612038123 (2026).

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A new explainer from berkeley.edu's Evo in the News:
- Human evolution and the humble potato : berkeley.edu

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One of the study's authors previously shared the May 2026 study here:
- New paper on evolution of starch digestion in Andeans : evolution subreddit

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• University of Vienna press release:
  • Roadmap of animal biodiversity: largest-ever comparison of chromosome-scale genomes
• Paper:
  • Schultz, D. T., Blümel, A., Destanović, D., Sarigol, F., & Simakov, O. (2026). Topological mixing and irreversibility in animal chromosome evolution. Science Advances.
    https://www.science.org/doi/10.1126/sciadv.adz5561
    From which:

> ... Our approach shows that irreversible genomic changes, caused in particular by chromosomal consolidation, dissociation, and fusion-with-mixing, place clades in distinct regions of genome architecture space. Progressive accumulation of these mixed states across genomic scales contributes to the diverging paths of animal genome evolution and has a long-lasting impact on a broad range of genes, including key developmental loci.

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Related: Evolutionary History of Mammalian Ancestor Chromosomes (Damas et al 2022) : evolution

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Cool result from today! The abstract:

Background

> Escherichia coli is a prototroph and can synthesize all twenty proteinogenic amino acids when required to grow in minimal medium. There are approximately sixty protein-coding genes individually essential for amino acid synthesis. This is a large mutational target for the accumulation of detrimental mutations. E. coli can rewire biosynthetic pathways in response to mutational damage, but the limits of this capacity are poorly understood.

Methods

> Here, to address evolutionary robustness, we asked whether and how the phenotypes of irreversible mutations causing auxotrophy could be suppressed or bypassed in the absence of horizontal gene transfer (HGT).

Results

> Spontaneous suppressors could be selected for only ten of fifty-nine mutants tested (detection limit ∼7x10^(-11)). Mechanisms of suppression included: regional amplifications; mutations increasing gene or operon expression; mutations relaxing enzyme specificity; and mutations causing biochemical pathway diversions.
Overall, the data show that spontaneous suppression of auxotrophy caused by an irreversible mutation is an evolutionary survival mechanism relevant only to a minority of the genes essential for amino acid synthesis. As a consequence, the essential genetic foundations for amino acid prototrophy are expected to be degraded over time by mutations (Muller’s ratchet) and metabolic rewiring alone will be insufficient to counteract this effect.

Discussion

> This implies that maintaining phenotypes, including prototrophy in E. coli, and potentially other bacterial species, is likely to be reliant on HGT of housekeeping genes to counteract the effects of inevitable mutational inactivation. Accordingly, chromosomal HGT in bacteria may be critical for survival across diverse environmental niches.

• Otto Lindahl, Talía Berruga-Fernández, Jivanti Soekhoe, Douglas L Huseby, Diarmaid Hughes
  The evolutionary maintenance of amino acid prototrophy in Escherichia coli
  Genome Biology and Evolution, 2026;, evag209
  https://doi.org/10.1093/gbe/evag209

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I think "may be critical for survival across diverse environmental niches" is underselling it!
Given 1) this result, 2) that we don't synthesize 9 of the essential amino acids,^([1]) and 3) how the secondary (non-naturally occurring) amino acids for a total of 20 had to evolve during the evolution of the genetic code, which is suggested to have been under selection for a reduction in code ambiguity,^([2]) then HGT would be indispensable for the evolution as well as maintenance of Metazoa and company.
Over to you.

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1: Costa, Igor R., et al. "Metazoan remaining genes for essential amino acid biosynthesis: sequence conservation and evolutionary analyses." Nutrients 7.1 (2014): 1-16. https://doi.org/10.3390/nu7010001

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

That's a low-res of one of the winning images:

> In 2026, researchers around the world participated in a joint image competition hosted by BMC Ecology and Evolution and BMC Zoology. Their photographs highlight the beauty and diversity of nature, showcasing the remarkable efforts of scientists to understand and protect it. This Editorial presents the winning images, selected by the Editor and senior members of the journals’ Editorial boards.

Article: 2026 joint BMC Ecology and Evolution and BMC Zoology image competition: the winning images | BMC Ecology and Evolution | Springer Nature Link

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Published yesterday in Molecular Biology and Evolution.

A few days ago there was this headline: This 236-Million-Year-Old Fossil Might Rewrite Mammals' Evolutionary History.
By coincidence, Álvarez-Carretero et al.'s timely paper (which addresses mammals) suggests that such "rewritings" have never been necessary, rather are to be expected of fossil finds:

Background

> The fossil record is incomplete, as evidenced by the pervasive presence of ghost lineages throughout the Tree of Life. For example, across placental mammals, at least 720 Myr of basal lineages are ghost lineages, that is, lineages that have left no fossil evidence of their past history. In contrast, some studies have suggested that the fossil record is a faithful temporal archive of evolutionary history and thus the times of diversification of clades must be close to the ages of their oldest fossils.
Such literalist interpretations have been contradicted by analysis of molecular data sets which, in many cases, indicate that groups including placental mammals and animals may have originated at times substantially older than their fossil records. Some of those studies have further argued that, in the case of animals and placental mammals, molecular clocks are uninformative, suffer from characteristic pathologies, and thus cannot distinguish between recent and ancient hypotheses of diversification.

Methods and results

> Here, we re-examine these two cases and show, using Bayesian model selection theory, that the explosive diversification models previously proposed for animals and placental mammals have a posterior probability of ∼0. We show the characteristic pathologies purportedly discovered do not exist, highlight errors in previous analyses, and provide advice on best practice for molecular-clock dating analysis.

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The paper discusses why such analyses weren't possible before, but I leave the details to the pros here - any insights are appreciated! (Also there's spicy drama in the paper / science working as advertised.)

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• Sandra Álvarez-Carretero, Ziheng Yang, Philip C J Donoghue, Mario dos Reis
  On the Origin of Animals and Placental Mammals: A Critique of Literalist Readings of the Fossil Record
  Molecular Biology and Evolution, 2026;, msag211
  https://doi.org/10.1093/molbev/msag211

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)

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• 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.

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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

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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.

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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.

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.

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