The research team, led by scientists working on deep-sea echinoderms, sequenced the mitochondrial genomes of four brittle star species collected from deep-sea environments: Ophioctenella acies, a hydrothermal vent dweller; Ophiura cf. irrorata and Ophiactis profundi, both from non-reduced deep-sea habitats; and Ophiocreas nudusoralis. Notably, the mitochondrial genome of O. acies represents the first ever reported from a hydrothermal vent ophiuroid, filling a significant gap in our understanding of how life thrives at these chemically extreme undersea hot springs.

Mitochondrial genomes are compact circular DNA molecules inherited maternally, making them powerful tools for reconstructing evolutionary relationships. Using next-generation sequencing on an Illumina NovaSeq 6000 platform, the researchers extracted genomic DNA from specimens preserved in ethanol, assembled the circular mitogenomes with the NOVOPlasty assembler, and annotated them with the MITOS2 toolset. The four new genomes ranged in length from 15,850 to 16,326 base pairs and contained the standard set of 37 mitochondrial genes, including 13 protein-coding genes, two ribosomal RNA genes, and 22 transfer RNA genes.

With these new sequences in hand, the team employed maximum likelihood and Bayesian inference approaches to reconstruct the phylogeny of the entire class. The resulting trees, generated independently by three different methods, consistently supported the monophyly of the two major clades within Ophiuroidea, Ophintegrida and Euryophiurida, as well as the four major orders: Ophiurida, Euryalida, Amphilepidida, and Ophiacanthida. This is a significant achievement, as the monophyly of Amphilepidida and Ophiacanthida had remained controversial in previous analyses, with different datasets and methods yielding up to nine distinct topologies among 18 generated trees in earlier work.

The improved phylogenetic resolution also clarified previously unstable family-level relationships. Within Euryalida, the study confirmed that Asteronychidae clusters with Gorgonocephalidae rather than occupying a basal position, consistent with some prior molecular studies. Within Ophiurida, the relationships among species in the families Ophiuridae and Ophiopyrgidae remain complicated, with the genus Ophiura showing some conflicts with earlier classifications. The authors suggest that an integrated review combining morphological and molecular evidence is urgently needed to fully resolve these remaining uncertainties.

Beyond phylogeny, the study delved into the temporal history of brittle star evolution. Using BEAST software with seven fossil-based calibration points and an uncorrelated relaxed molecular clock, the researchers estimated that the common ancestor of all Ophiuroidea originated around the Permian-Triassic boundary, approximately 255 million years ago, coinciding with the most severe mass extinction event in Earth’s history. The four major orders radiated at different times: Ophiacanthida and Amphilepidida emerged during the Triassic, Ophiurida during the Jurassic, and Euryalida more recently in the Cretaceous.

The ancestral state reconstruction revealed a fascinating pattern of bidirectional habitat transitions between shallow and deep waters. Ophiacanthida and Euryalida appear to have originated in the deep sea and repeatedly colonized shallow environments, while Ophioleucida and Ophiurida expanded from shallow waters into the deep. These transitions were particularly concentrated during the Jurassic and Cretaceous periods, coinciding with major geological events such as plate tectonic movements, the formation of new marine basins, rising deep-sea temperatures that reduced the thermal gradient between surface and bottom waters, and significant sea level rise. The mid-Cretaceous divergences may be linked to repeated oceanic anoxic events and warm geological intervals that reshaped ocean chemistry and ecology.

One of the most intriguing findings concerns the colonization of chemosynthetic ecosystems, such as hydrothermal vents and cold seeps, which are oases of life in the otherwise food-scarce deep sea. The study found that among four chemosynthetic species analyzed, three experienced significant fluctuations in marine sulfate levels just prior to their divergence, suggesting a possible link between sulfur chemistry and the evolution of vent and seep fauna. The cold-seep species Histampica haimaensis was the first to diverge in the mid-Jurassic, followed by Amphiura sp. in the early Cretaceous, while Ophiophthalmus serratus and Ophioctenella acies diverged in the early Paleogene.

When the researchers examined adaptive evolution at the molecular level, they found a surprising contrast between the hydrothermal vent species and the cold-seep species. The three cold-seep brittle stars showed clear evidence of mitochondrial gene rearrangements and positive selection on specific genes, including ATP6, ATP8, ND2, COX1, and COX2, consistent with adaptive responses to the toxic, oxygen-poor conditions of their environments. However, the hydrothermal vent species O. acies showed no gene rearrangements and no positive selection signals, instead exhibiting the lowest nucleotide substitution rates among the four species, suggesting it may have adapted through strong purifying selection that minimizes the accumulation of harmful mutations rather than through the evolution of new molecular functions.

This finding challenges the assumption that extreme environments universally drive positive selection in mitochondrial genomes and highlights the diversity of evolutionary strategies that organisms can employ when colonizing harsh habitats. The study also revealed that mitochondrial gene rearrangement patterns and selective pressures varied markedly between lineages rather than correlating with habitat type or depth, with the clade Ophintegrida showing higher structural plasticity than the more conserved Euryophiurida. By establishing the most comprehensive mitochondrial genome framework for brittle stars to date, this research provides a robust foundation for future investigations into echinoderm diversification, biogeographic dispersal, and the molecular mechanisms that enable life to flourish in some of the most extreme environments on our planet.

Subject of Research: Mitochondrial genome phylogenetics and deep-sea adaptive evolution of brittle stars (Ophiuroidea)

Article Title: Mitochondrial genomes resolve phylogenetic conflicts and lineage-specific adaptive dynamics in Ophiuroidea : insights from deep-sea lineages

Article References: Xu, W., Na, J., Gao, K., Gu, X., Zhou, Y., Zhang, R., Sun, J., & Zhang, D. (2026). Mitochondrial genomes resolve phylogenetic conflicts and lineage-specific adaptive dynamics in Ophiuroidea: insights from deep-sea lineages. Zoosystematics and Evolution, 102(2), 687-699. https://doi.org/10.3897/zse.102.163746

Image Credits: AI Generated

DOI: 10.3897/zse.102.163746

Keywords: brittle stars, Ophiuroidea, mitochondrial genomes, deep sea, hydrothermal vents, cold seeps, phylogenetics, adaptive evolution, echinoderms, gene rearrangement, positive selection, divergence time

The six newly sequenced species—B. repanda, B. axillaris, B. sinuata, B. martiniana, B. megacephala, and B. formosana—were collected from Yunnan Province in southwestern China, where more than half of the country’s Blumea species have documented medicinal uses. Among them, B. balsamifera, known locally as Dafeng’ai, has been used for thousands of years across China and Southeast Asia to treat eczema, dermatitis, beriberi, menorrhagia, and skin injuries. Modern pharmacological studies have identified L-borneol as its primary bioactive constituent, and the species holds a special place in traditional Chinese medicine as the only botanical source of Aipian, a substance used to clear orifices and invigorate the spirit. Other species such as B. megacephala, B. riparia, B. aromatica, B. formosana, and B. densiflora have likewise demonstrated considerable pharmacological potential.

Chloroplasts are the photosynthetic powerhouses of plant cells, and their genomes typically measure between 115 and 165 kilobases in a conserved quadripartite structure: a large single-copy region, a small single-copy region, and two inverted repeats. Because chloroplast DNA is maternally inherited, lacks recombination, and has a reduced effective population size, it is a stable and reliable tool for reconstructing plant evolutionary relationships. Advances in next-generation sequencing have made plastid genome assembly cheaper and faster, accelerating phylogenomic studies across diverse taxonomic scales. The research team used the Illumina HiSeq 2500 platform to generate 150-base-pair paired-end reads, filtered low-quality data with Fastp, and assembled complete plastomes with GetOrganelle, verifying each sequence by alignment against the reference genome of B. balsamifera.

The resulting plastomes ranged from 150,783 base pairs in B. sinuata to 151,281 base pairs in B. formosana, all falling within the typical size range for most angiosperms. Each contained the canonical quadripartite architecture, with inverted repeats measuring 24,924 to 24,957 base pairs, a large single-copy region of 82,524 to 82,894 base pairs, and a small single-copy region of 18,355 to 18,509 base pairs. Overall GC content was nearly constant across species at 37.5 to 37.6 percent, with the inverted repeats showing the highest GC content at 43 percent, followed by the large single-copy region at 35.6 to 35.7 percent and the small single-copy region at 30.8 to 31.0 percent. Each plastome contained 131 genes, including 8 ribosomal RNAs, 37 transfer RNAs, and 86 protein-coding genes, 18 of which were duplicated within the inverted repeats.

Whole-genome alignments with Mauve revealed no detectable gene rearrangements or inversions across all ten plastomes, confirming that Blumea’s chloroplast genome evolution has been relatively conservative. Sequence identity analysis using mVISTA confirmed that inverted repeats are more conserved than single-copy regions and that coding regions are more conserved than non-coding ones. Nucleotide diversity estimates yielded the same pattern: in non-coding regions, variation spanned 0.19 to 8.36 percent with a mean of 3.82 percent, averaging 4.21 percent in the large single-copy region, 0.87 percent in the inverted repeats, and 6.25 percent in the small single-copy region. In coding regions, variation ranged from 0 to 3.70 percent with a mean of 1.25 percent. Non-coding regions diverged 3.06-fold more than coding regions overall.

Six non-coding regions showed over 6 percent variability—trnH-psbA, rps16-trnQ-UUG, atpI-atpH, ycf4-cemA, ndhG-ndhI, and rps15-ycf1—making them candidate DNA barcodes for genus-level phylogenetic studies. Four genes—ycf1, rps8, ndhF, and matK—showed the highest variability among coding regions. Comparison of the inverted repeat and single-copy boundary positions across the ten plastomes revealed generally conserved inverted repeat regions along with limited structural variation at specific junctions. At the large single-copy and inverted repeat b boundary, rps19 sits in the large single-copy region 10 to 13 base pairs from the junction, while rpl2 resides in the inverted repeat b region 52 to 60 base pairs away. A truncated copy of ycf1 straddles the inverted repeat b and small single-copy junction, extending 0 to 21 base pairs into the small single-copy region in nine species; in B. balsamifera, this copy is pseudogenized. The intact ycf1 copy in the small single-copy region extends 564 to 581 base pairs into the inverted repeat a region across the small single-copy and inverted repeat a junction.

The research team also catalogued repetitive sequences across the ten plastomes, identifying 395 dispersed repeats comprising 181 forward, 202 palindromic, 11 reverse, and one complementary repeat. B. axillaris exhibited the highest number at 49, while B. martiniana had the fewest at 34. Forward and palindromic repeats were present in all species, reverse repeats were detected in six species, and complementary repeats were exclusive to B. tenella. Most dispersed repeats were located in the large single-copy and inverted repeat regions, with the majority residing in intergenic spacers. Repeats of 30 to 39 base pairs were the most abundant, followed by those of 40 to 49 base pairs. In addition, 79 tandem repeats and 547 simple sequence repeats were identified across the ten plastomes. Mononucleotide repeats were the most abundant at 425, accounting for 77.70 percent of all SSRs, and among mononucleotide SSRs, A/T motifs overwhelmingly dominated over G/C motifs at 417 versus 8. B. formosana exhibited the highest number of SSRs at 63, and B. martiniana the lowest at 50.

Codon usage analysis of 52 filtered coding sequences revealed identical patterns across all ten plastomes, with 29 codons showing frequent usage and 28 of those ending in A or U, while 30 codons were used less frequently and 28 of those ended in C or G. The codon UUA encoding leucine exhibited the highest relative synonymous codon usage value at 1.89 to 1.94, whereas AGC encoding serine showed the lowest at 0.32 to 0.33. Leucine was the most abundant amino acid at 10.97 to 11.07 percent of all codons, and cysteine was the least abundant at 1.12 to 1.16 percent. This strong preference for A/U-ending codons is consistent with numerous angiosperm plastomes and provides critical insight into the molecular evolutionary mechanisms underlying Blumea’s plastid genomes.

Phylogenetic trees reconstructed from 79 shared protein-coding genes across 23 taxa, with two Helianthus species as outgroups, divided the 21 Inuleae species into four major clades. All ten Blumea species formed a highly supported monophyletic group, internally divided into three subclades. Subclade I comprised six species—B. axillaris, B. oxyodonta, B. megacephala, B. repanda, B. sinuata, and B. tenella—within which B. sinuata was sister to B. tenella and B. megacephala was sister to B. repanda. Subclade II consisted of a single species, B. balsamifera, which formed a sister lineage to Subclade I. Subclade III comprised three species—B. aromatica, B. formosana, and B. martiniana—with B. martiniana as the basal taxon and B. aromatica sister to B. formosana. Notably, all three species of Subclade III belong to Section Macrophylla, and the Bayesian inference tree topology was entirely congruent with the maximum likelihood tree for the ten Blumea species.

Positive selection analysis using the MEME method identified 21 genes containing significant episodic positively selected sites along the Blumea lineage, while the FUBAR method detected no pervasive positive selection, indicating that the signals represent lineage-specific events. Among the 21 candidate genes, ycf1 contained the highest number of positively selected sites at 75, followed by ycf2 at 17 and rpoB at 7. These genes are primarily involved in photosynthesis, energy metabolism, gene transcription, and protein synthesis. Photosystem I genes psaA and psbB, photosystem II gene psbA, ATP synthase genes atpA and atpF, and cytochrome b6f complex gene petA support the overall optimization of photosynthetic electron transport and energy metabolism. Multiple NADH dehydrogenase complex genes—ndhA, ndhB, ndhD, ndhF, and ndhG—and the acetyl-CoA carboxylase gene accD are involved in cyclic electron transport and fatty acid synthesis, respectively. Blumea species are predominantly distributed in tropical and subtropical open habitats, exhibiting strong adaptability to varying light environments, and their relatively high photosynthetic efficiency and broad light adaptation range are consistent with the positive selection observed in these photosynthesis-related genes. The ycf1 and ycf2 genes encode key components of the plastid inner envelope protein transport complex, with Ycf1 potentially serving as the protein translocation channel and Ycf2 providing ATPase activity to energize the transport process. These two genes harbored the highest number of positively selected sites in Blumea, suggesting they may play important roles in the adaptive evolution of the genus and even the Asteraceae family. The mixed life forms within subclades—annuals such as B. tenella and B. axillaris alongside perennials such as B. megacephala—suggest that the evolution of life-history strategies in this genus may be more complex than previously recognized, and the unique phylogenetic position of B. balsamifera may indicate it has undergone a different evolutionary history from other Blumea species, possibly retaining ancestral traits. The identified SSRs and candidate barcodes may facilitate molecular marker development and population genetics, providing a genomic foundation for future studies on the phylogeny and adaptive evolution of this medicinally important genus.

Subject of Research: Comparative chloroplast genome analysis and phylogenetic relationships of ten Blumea species in the Asteraceae family

Article Title: Plastomes of Ten Blumea Species (Asteraceae): Comparative Analysis and Phylogenetic Relationships

Article References: Zhao, Y., Yang, W., Qian, C., Zhou, T., Zhang, X., Chen, X., Zhang, R., & Liu, X. (2026). Plastomes of Ten Blumea Species (Asteraceae): Comparative Analysis and Phylogenetic Relationships. Ecology and Evolution, 16(10), Article e74361. https://doi.org/10.1002/ece3.74361

Image Credits: AI Generated

DOI: 10.1002/ece3.74361

Keywords: Blumea, Asteraceae, chloroplast genome, plastome, phylogenetics, positive selection, Inuleae, SSRs, codon usage, DNA barcodes, Balsamifera, Yunnan China

The mitochondrial genome of A. imberbis spans 16,576 base pairs, a length squarely within the typical 16 to 17 kilobase range for vertebrates. It contains the standard vertebrate mitogenomic toolkit: 13 protein-coding genes, 22 transfer RNA genes, two ribosomal RNA genes, and a non-coding control region. Nucleotide composition analysis revealed a strongly AT-rich genome, with adenine and thymine together accounting for 58.93 percent of all bases. Guanine was distinctly deficient at just 15.88 percent, a bias consistent with what has been observed in typical bony fish mitochondrial genomes and a hallmark of vertebrate mitogenomic architecture.

Gene arrangement followed the conserved pattern seen across most Cyprinidae. Of the 37 encoded genes, 28 sit on the heavy strand while nine, including the ND6 gene and eight tRNA genes, occupy the light strand. Four gene overlaps were identified, three between protein-coding genes, namely ATP8/ATP6 at 6 base pairs, ND4L/ND4 at 7 base pairs, and ND5/ND6 at 4 base pairs, plus a 2-base-pair overlap between tRNA-Ile and tRNA-Gln. Twelve intergenic spacers ranging from 1 to 31 base pairs were found, with the longest gap between tRNA-Asn and tRNA-Cys. The control region, or D-loop, measured 915 base pairs and showed a pronounced A+T preference of 65 percent, reinforcing the anti-guanine tendency typical of fish mitochondrial DNA.

Among the 13 protein-coding genes, COI stood out by using GTG, which encodes valine, as its initiation codon, a feature prevalent among non-tetrapod vertebrates. The remaining 12 genes all began with ATG, encoding methionine. Stop codons varied considerably: complete TAA codons appeared in seven genes, TAG in two, while ND4 carried the incomplete TA and COII, COIII, and Cyt b ended with a single T, presumably completed by post-transcriptional polyadenylation. Codon usage analysis revealed a preference for leucine and alanine, and the relative synonymous codon usage showed that codons ending in A at the third position were used more frequently than expected by chance.

The 22 tRNA genes, totaling 1,561 base pairs, ranged from 67 to 76 base pairs in length and folded into the classic cloverleaf secondary structure with amino acid-accepting, dihydrouridine, anticodon, and TΨC arms plus a variable loop. Two copies each of tRNA-Ser and tRNA-Leu were present, while all other tRNAs appeared once. Notably, tRNA-Ser (AGY) lacked the DHU arm entirely, accompanied by UG and UC mismatches, a nucleotide-economy feature also seen in other cyprinids. The two rRNA genes, 12S at 963 base pairs and 16S at 1,683 base pairs, sat between tRNA-Phe and tRNA-Leu, separated by tRNA-Val.

Within the control region, the team identified several conserved motifs critical for mitochondrial replication and transcription, including the extended termination-associated sequence, the central conserved domain containing CSB-F, CSB-E, and CSB-D, and the conserved sequence blocks CSB-1, CSB-2, and CSB-3. A short TA tandem repeat was detected, and a brief AT duplication occurred between positions 798 and 812. Such insertions and deletions can generate different haplotypes, hinting at the structural plasticity that makes the control region a hotspot for evolutionary studies.

To place A. imberbis in its evolutionary context, the researchers constructed a maximum likelihood phylogenetic tree using concatenated sequences of all 13 protein-coding genes from 37 species, including five outgroup taxa. The best-fitting substitution model, TIM2+F+R4, was selected under the Bayesian Information Criterion, and branch confidence was assessed with 5,000 ultrafast bootstrap replicates. The tree robustly confirmed the monophyly of Acheilognathinae, which split into two primary clades: one containing Acheilognathus and the other comprising the Tanakia–Rhodeus complex. This two-clade structure provides a clearer framework than earlier analyses based on short mitochondrial fragments, which had yielded inconsistent results for the genera Tanakia and Rhodeus.

However, the phylogeny also exposed cracks in current taxonomy. Rhodeus ocellatus and Rhodeus lighti clustered together as a strongly supported sister group that diverged before the split between the core Tanakia and Rhodeus lineages, while Pseudorhodeus tanago nested within the Rhodeus/Pseudorhodeus clade. Most strikingly, Rhodeus albomarginatus was placed within the Acheilognathus clade rather than grouping with other Rhodeus species, an anomalous position the authors urge readers to interpret cautiously given that only a single complete mitochondrial genome of this species is currently available. The monophyletic status of Rhodeus received limited nodal support overall, suggesting that generic boundaries within the subfamily may not fully reflect evolutionary history and that taxonomic revisions could be on the horizon.

Genetic distance analysis using the Tamura–Nei model revealed substantial heterogeneity across the subfamily, with pairwise distances ranging from 0.0071 to 0.2600. The closest relative to A. imberbis was Acheilognathus meridianus at a distance of 0.1153, followed by A. yamatsutae at 0.1461. More provocatively, Acheilognathus gracilis and Acheilognathus rhombeus clustered together on the tree yet showed a genetic distance of only 0.0071, far below the 0.0406 threshold generally associated with significant species or subspecies differentiation in mitochondrial cytochrome b studies. Similarly low divergences appeared between Rhodeus suigensis and R. notatus (0.0162) and between R. suigensis and R. fangi (0.0153). These findings suggest that some nominal bitterling species may warrant re-evaluation using integrative taxonomic approaches that combine molecular, morphological, and ecological evidence.

Positive selection analysis of the ND2 gene, conducted across 29 species using six codon-based site models in PAML, detected no statistically significant codon positions under adaptive evolution. Likelihood ratio tests between nested models showed that while the discrete and beta-plus-omega models fit better than simpler alternatives, the Bayes Empirical Bayes analysis yielded no sites with posterior probabilities of omega exceeding 1 above the 0.95 significance threshold. This absence of positively selected sites indicates that ND2 has evolved predominantly under purifying selection within Acheilognathinae, consistent with the functional constraints on oxidative phosphorylation genes and the relatively stable thermal and ecological conditions these fish inhabit. The result underscores the conservative nature of mitochondrial energy metabolism genes and suggests limited lineage-specific adaptive divergence in this group. Taken together, the complete mitogenome of A. imberbis enriches the molecular resources available for bitterling systematics, sharpens the subfamily’s phylogenetic framework, and highlights both the power and the limits of mitochondrial inference, pointing toward future studies that incorporate nuclear genomic data and broader taxon sampling to achieve a more stable understanding of bitterling evolution.

Subject of Research: Mitogenomics and phylogeny of the bitterling fish Acheilognathus imberbis

Article Title: Mitogenomic architecture of Acheilognathus imberbis ( Actinopterygii , Cypriniformes , Cyprinidae ): Implications for Acheilognathinae phylogeny

Article References: Liu, G., Peng, D., Zhang, H., Song, D., Liu, B., & Cheng, Q. (2026). Mitogenomic architecture of Acheilognathus imberbis (Actinopterygii, Cypriniformes, Cyprinidae): Implications for Acheilognathinae phylogeny. Acta Ichthyologica et Piscatoria, 56, 181-194. https://doi.org/10.3897/aiep.56.181178

Image Credits: AI Generated

DOI: 10.3897/aiep.56.181178

Keywords: mitochondrial genome, Acheilognathus imberbis, bitterling, phylogenetics, Acheilognathinae, Cyprinidae, genetic distance, positive selection, ND2 gene, taxonomic revision, Mitogenomic, architecture

A team led by Shao’e Sun, Min Hui, Jin Sun and Zhongli Sha has assembled the first near-telomere-to-telomere genome of the coral reef-dwelling feather star Cenometra bella, a crinoid that thrives in one of the most environmentally volatile habitats in the ocean. The genome spans 354.7 megabases organized into just 12 chromosomes, and it was built from long Pacific Biosciences HiFi reads scaffolded with Hi-C chromosome conformation capture data. The result is an assembly of remarkable quality: a contig N50 of 28.25 megabases, meaning half the genome resides in contiguous sequences longer than that, and a completeness score of 97.5 percent against the BUSCO set of universal single-copy genes. Using the Genome Continuity Inspector metric, the assembly achieved a GCI score of 75.0837, placing it well above all previously published crinoid genomes.

Telomere-to-telomere assemblies are the gold standard of genomics because they aim to read each chromosome end to end, resolving the repetitive telomeric caps, the dense centromeric cores, and everything in between. For crinoids, this level of resolution has been a long time coming. The group has historically lacked high-quality genomic resources, leaving a conspicuous gap in our understanding of how the earliest echinoderm lineages evolved at the DNA level. By precisely identifying the telomeric repeats and centromeric regions of C. bella, the researchers could anchor genes with confidence and highlight those sitting near these structurally critical regions. Many of these genes are involved in intracellular metabolism, signal transduction and the regulation of the nervous system, hinting that genomic architecture around centromeres and telomeres may carry functional significance beyond structural housekeeping.

The most striking finding, however, lies in how the 12 chromosomes of C. bella relate to the ancestral echinoderm blueprint. Earlier work on other echinoderms had inferred a set of 23 ancestral linkage groups, the hypothetical chromosome set from which modern sea stars, sea urchins, sea cucumbers and their relatives descend. Through macrosynteny analysis, a technique that tracks how blocks of genes stay together on chromosomes across hundreds of millions of years of evolution, the team uncovered nine chromosomal fusion events. Nine separate ancestral linkage groups had been stitched together in various combinations to compress the presumed 23 into the 12 chromosomes observed today. This is the highest degree of chromosomal fusion ever documented in an echinoderm, and the authors suggest it may represent a genuine evolutionary innovation within the phylum.

Fusions of this magnitude are not merely a curiosity of genome bookkeeping. When chromosomes merge, genes that were once regulated separately can come under shared chromosomal environments, and topological association domains, the self-interacting loops of chromatin that organize the genome inside the nucleus, can be rearranged. The researchers asked what kinds of genes ended up on the fused chromosomes and found a telling pattern: genes on these chromosomes were functionally enriched in attachment-related processes such as cell adhesion, energy metabolism, environmental sensing and immune response. For an animal that must anchor itself firmly to reef substrates while filtering food from moving water, and that must cope with the daily swings of a coral reef environment, that collection of functions reads almost like a survival toolkit.

Coral reefs are punishing places to live. Ultraviolet radiation near the surface can damage DNA and generate reactive oxygen species, temperatures can swing across a diurnal and seasonal range, and pathogens flourish in warm, nutrient-rich waters. The comparative genomic analysis of C. bella points to several molecular strategies that may underlie the species’ tolerance of these stresses. The team identified 28 expanded gene families, encompassing 455 genes, as well as 194 positively selected genes, detected through elevated ratios of non-synonymous to synonymous substitutions. The functions of these gene sets converge on three themes: lipid synthesis, DNA repair and membrane stability. Enhanced lipid production and membrane maintenance could help the animal keep its cell membranes fluid under thermal stress, while bolstered DNA repair machinery would counteract the mutational pressure of intense ultraviolet exposure in shallow reef waters.

What makes these findings conceptually important is the contrast they create with the traditional picture of crinoid evolution. Crinoids are famous for their exceptionally slow rates of morphological and molecular evolution, a conservatism so pronounced that they serve as a benchmark for studying evolutionary stasis. The C. bella genome does not overturn that reputation, but it complicates it. Stability in body form, it appears, does not preclude dramatic rearrangement of the genome itself. The nine fusion events show that while the animal’s arms, calyx and overall architecture have remained strikingly faithful to ancient designs, its chromosomes have undergone wholesale consolidation. Evolution, in other words, can be radical at one level of biological organization while remaining conservative at another.

Methodologically, the study also raises the bar for echinoderm genomics. Previous crinoid assemblies were fragmentary, leaving genes scattered across thousands of small scaffolds and making it difficult to study chromosome-scale evolution. The near-T2T assembly of C. bella, with its long contigs, resolved centromeres and identified telomeric repeats, provides the kind of reference genome against which other echinoderm genomes can be compared chromosome by chromosome. Because synteny is such a powerful lens for reconstructing deep evolutionary history, having a crinoid genome of this quality matters for the entire phylum: it helps clarify which chromosome-scale features are ancestral to all echinoderms and which, like the fusions seen here, are innovations of particular lineages.

The adaptive story remains, as the authors are careful to note, a suggestion rather than a demonstration. Expanded gene families and positively selected genes associated with lipid synthesis, DNA repair and membrane stability are consistent with life in a fluctuating reef environment, but confirming those roles will require functional work, perhaps gene expression studies across environmental gradients or experiments exposing the animals to controlled UV, thermal and pathogen challenges. Still, the correlation between the fused chromosomes and genes governing attachment, metabolism, sensing and immunity offers a compelling hypothesis: that genome restructuring itself may have been part of how this lineage carved out a niche in the dynamic coral reef ecosystem.

For a phylum that has survived four hundred and eighty million years of planetary upheaval, the feather star has now offered up one of its deepest secrets at the highest resolution yet achieved. Cenometra bella, swaying gracefully above the reef, carries in its 12 compact chromosomes a record of both extraordinary stability and extraordinary change. As telomere-to-telomere technology spreads through comparative genomics, more living fossils are likely to yield similar surprises, and the textbook image of crinoids as frozen in time may give way to something far more interesting: organisms whose outward stillness conceals genomes that have never stopped moving.

Subject of Research: Near-telomere-to-telomere genome assembly and chromosome evolution of the feather star Cenometra bella

Article Title: The near-T2T genome of the feather star Cenometra bella suggests potential evolutionary innovations and coral reef habitat tolerance

Article References: Sun, S., Hui, M., Sun, J., & Sha, Z. (2026). The near-T2T genome of the feather star Cenometra bella suggests potential evolutionary innovations and coral reef habitat tolerance. BMC Genomics. https://doi.org/10.1186/s12864-026-13458-4

Image Credits: AI Generated

DOI: 10.1186/s12864-026-13458-4

Keywords: crinoids, feather star, Cenometra bella, telomere-to-telomere genome, genome assembly, chromosome fusion, macrosynteny, echinoderm, coral reef, gene family expansion, positive selection, DNA repair

The pig family is an unusually valuable model for studying immune evolution. Suids occupy a remarkable range of ecological niches, from the forests and farms where domestic pigs live to the arid savannas inhabited by warthogs and bushpigs. Alongside this ecological breadth comes wide variation in disease susceptibility. African wild suids can tolerate infections that devastate domestic pigs, and understanding the genetic basis of such differences has long been a goal for evolutionary biologists and veterinary researchers alike. Yet before this study, no systematic cross-species survey of immune gene variation had been carried out across the family.

To build their dataset, the team first compiled a high-confidence set of 1,946 conserved mammalian immune-related genes. These genes, drawn from established annotation frameworks, span the major arms of the immune system, including innate recognition, inflammatory signaling, and adaptive responses. The researchers then mapped whole-genome sequencing reads from the 12 suid species against these genes, calling single-nucleotide variants and small insertions and deletions with careful quality filtering. Stringent filters based on metrics such as read depth, strand bias, and variant quality ensured that the variants used in downstream analyses were unlikely to be sequencing artifacts.

From this foundation, the team searched for what they term critical variants: mutations predicted to cause the gain or loss of start or stop codons, frameshifts, or disruptions of splice sites. Such mutations can profoundly alter protein function. Across the 12 species, the analysis identified 51 genes carrying 62 lineage-specifically fixed critical variants, meaning the damaging allele is present in all members of one lineage while absent from the others. Among these, 21 events were classified as putative loss-of-function mutations, disrupting more than half of the protein-coding sequence of the affected gene.

One of the most notable findings concerns the interleukin-1 gene family, a cluster of genes central to inflammation and innate immunity. The study found evidence of progressive degeneration within this family across suid evolution, with different lineages showing different degrees of decay. Degenerating gene families are a well-known feature of genome evolution, but their occurrence in a family of genes as immunologically important as the interleukin-1 cluster suggests that some inflammatory functions may have been relaxed or reshaped in particular suid lineages, potentially altering how these animals mount fever and inflammatory responses to infection.

African suids emerged as a particularly distinctive case. Warthogs, bushpigs, and forest hogs showed unique evolutionary signatures in innate immune and inflammatory pathways, including the apparent inactivation of the CD177 gene. CD177 encodes a protein expressed on a subset of neutrophils, the white blood cells that form the first line of defense against bacterial and fungal pathogens, and it has been implicated in inflammatory regulation in other mammals. Its inactivation in African suids hints at a rewiring of neutrophil biology in these species, although the precise functional consequences will require experimental follow-up.

In contrast, the Sus lineage, which includes domestic pigs and wild boars, harbored fewer disruptive variants than the other suid lineages. Instead, it showed strong evidence of positive selection in genes associated with cytokine interactions and responses to infectious disease. Positive selection leaves a statistical footprint in coding sequences, detectable when the ratio of nonsynonymous to synonymous substitutions exceeds what neutral evolution would predict. In the Sus lineage, this signal concentrated in genes that mediate communication between immune cells, suggesting that the ancestors of pigs and boars experienced intense pathogen-driven pressure on the molecular machinery of immune signaling.

The recurrent appearance of immune gene inactivation across multiple, independent lineages is one of the study’s most thought-provoking results. Gene loss in the immune system can arise through genetic drift, particularly when a gene’s function becomes dispensable, but it can also be driven by positive selection, for example when losing a receptor deprives a pathogen of its entry point. The authors argue that both forces have shaped the suid immunome, with drift and selection combining in different measures across lineages to produce the diversity of immune gene repertoires observed today. Disentangling these contributions remains a central challenge in evolutionary immunology.

These findings carry practical implications beyond evolutionary theory. Domestic pigs are economically vital livestock and, at the same time, a reservoir and amplifier of pathogens with serious veterinary and public health consequences, including African swine fever virus, porcine reproductive and respiratory syndrome virus, and foot-and-mouth disease virus. African wild suids, which can host African swine fever virus without severe disease, represent natural experiments in tolerance that could illuminate resistance mechanisms. By pinpointing the immune genes that have been disrupted or positively selected in specific lineages, the study provides a shortlist of candidate loci for functional studies aimed at improving disease resistance and immune robustness in pigs.

The study also demonstrates the power of telomere-to-telomere era genomic resources and improved annotations when applied across non-model species. As reference genomes for wild suids continue to improve, the researchers expect the catalogue of lineage-specific immune variants to grow in resolution. For now, the work offers the first panoramic view of immune gene evolution across the pig family, revealing that even closely related mammals can take sharply divergent routes in building and pruning their immune systems, and that some of those routes may hold the keys to breeding healthier livestock.

Subject of Research: Comparative immunogenomics of immune gene evolution, loss-of-function variation, and positive selection across Suidae species

Article Title: Comparative immunogenomics of Suidae reveals lineage-specific immune gene disruption and positive selection

Article References: Shin, J. Y., Ahn, B., Kang, M., Dinka, H., Lee, J., Choi, M.-K., & Park, C. (2026). Comparative immunogenomics of Suidae reveals lineage-specific immune gene disruption and positive selection. BMC Genomics. https://doi.org/10.1186/s12864-026-13424-0

Image Credits: AI Generated

DOI: 10.1186/s12864-026-13424-0

Keywords: Suidae, immunogenomics, comparative genomics, loss-of-function mutation, positive selection, IL-1 gene family, CD177, African swine fever, innate immunity, host-pathogen coevolution, whole-genome sequencing, disease resistance

The research team focused on five large double-stranded DNA viruses: vaccinia virus, the type species of mammal-infecting poxviruses, and four human herpesviruses, namely herpes simplex virus 1, Epstein–Barr virus, human cytomegalovirus and Kaposi’s sarcoma-associated herpesvirus. These viruses are known to encode numerous host-like domains acquired through horizontal gene transfer during their long evolutionary history. To find them systematically, the researchers predicted the three-dimensional structures of 540 viral proteins using AlphaFold2 and then employed Foldseek, a fast structural homology search tool, to identify viral domains that structurally resemble human proteins. After a series of filtering steps designed to eliminate spurious matches between low-complexity folds and partially homologous structures, the pipeline yielded 7,593 human–viral structural homolog pairs derived from 144 distinct viral proteins.

The scale of this mimicry is striking. In herpes simplex virus 1, structurally host-like domains account for roughly 11 percent of the encoded proteome, while in vaccinia virus the figure rises to 31 percent. Notably, despite their structural resemblance, the sequence similarity between viral mimics and their human counterparts is often low, averaging just 28.4 percent within the homologous region and 6.3 percent across full-length proteins. This makes them imperfect mimics: similar enough in fold to bind the same partners, yet different enough in sequence that the interacting surfaces are not identical. The researchers then asked which of these structural homologs actually function in a similar way, defining functional similarity as the sharing of at least one common human interaction partner, which they termed a mutual host target.

By overlaying experimentally characterized human–virus protein interaction networks from databases such as HVIDB with within-human interaction maps from STRING, the team identified 645 triads consisting of a viral mimicking protein, a host-mimicked protein and a mutual host target. These triads involve 229 functionally mimicked human proteins, 40 viral mimicking proteins and 118 mutual host targets. One illustrative example is the KSHV protein ORF72, which structurally resembles the human cyclin CCNO, with both proteins predicted to interact with the human kinase CDK3 through a similar binding region. The set of functionally mimicked proteins, those with direct evidence of shared interactions, became the focus of the subsequent evolutionary analysis.

To measure evolutionary pressure, the researchers computed dN/dS, the ratio of nonsynonymous to synonymous substitutions, for more than 9,000 human genes across ten primate species, including chimpanzee, gorilla, orangutan, macaques and mouse lemur. The results were unambiguous. Human proteins known to bind viral proteins are significantly more conserved than the proteome at large, confirming earlier findings. But the proteins entangled in mimicry are conserved to an even greater degree. Mutual host targets, the human proteins contacted by both the viral mimic and the host-mimicked protein, were the most conserved viral-binding group tested, and functionally mimicked proteins were significantly more conserved than the broader set of structural homologs. When the team searched for signatures of pervasive positive selection using codon-based models in PAML, the picture was equally striking: proteins targeted by mimics showed virtually no positively selected genes at most statistical thresholds, in sharp contrast to the modest but detectable positive selection seen among viral-binding proteins in general.

What explains this exceptional conservation? The researchers found that mimicry-related host proteins sit at crowded hubs of the cellular interaction network. Mutual targets and functionally mimicked proteins have significantly more interaction partners than average human proteins, and targets of mimicry are also more highly expressed across tissues than other viral-binding proteins. Gene ontology analysis showed that these proteins are enriched in antiviral pathways such as cell death, cytokine response and inflammatory signaling, as well as in processes frequently manipulated by viruses, including Golgi regulation, the G1/S cell cycle transition and signal transduction. Within these shared functional categories, mimicked and target proteins were more conserved than their non-mimicked counterparts in the majority of cases, 75.6 percent for mimicked proteins and 63.2 percent for targets. The implication is that essential cellular roles constrain these proteins, leaving the host little room to mutate away from viral mimics without damaging its own interactome.

The analysis then zoomed in to the level of individual amino acids. Using AlphaFold-Multimer to predict complexes between mimicked and target proteins, the team identified interface residues and compared their evolutionary rates with those of buried core residues and exposed surface residues. As expected, interfaces and cores evolved more slowly than surfaces. More revealing was the comparison between two kinds of interface: mimicry interfaces, the residues that physically contact the mutual target, and general interfaces, predicted binding sites for unrelated proteins using the deep learning tool ScanNet and the SVM-based method ISPRED4. In both mimicked and target proteins, mimicry interfaces were significantly more conserved than general interfaces, indicating that the residues exploited by viral mimics are under especially strong purifying selection.

Because viral mimics are imperfect copies, their binding surfaces on the host target are not identical to those of the host-mimicked protein. The researchers therefore subdivided target interfaces into residues contacted by the host-mimicked protein, residues contacted only by the viral mimic, and residues contacted by both. The mutual residues were the most conserved, while residues exclusively touched by the viral protein evolved significantly faster. This pattern hints at a possible escape route: host surfaces used only by the virus, and not required for essential cellular interactions, may tolerate more change, potentially allowing the host to weaken viral interactions selectively. Yet even these faster-evolving regions showed no enrichment for positively selected residues, so the authors caution that this remains a hypothesis rather than demonstrated host escape. The team also compared perfect and imperfect mimicry, examining short linear motifs in disordered viral regions that exactly copy host motifs. Host proteins targeted by these perfect motif mimics, 89 in total, were the most conserved group in the entire study, more constrained even than targets of imperfect domain mimicry, consistent with the idea that perfect mimicry leaves the host no way to discriminate foe from friend.

On the viral side, the picture was more complex. Comparing orthologs across orthopoxviruses, simplexviruses, cytomegaloviruses and rhadinoviruses, the researchers found no consistent difference in evolutionary rate between mimicking and non-mimicking viral proteins, a result they attribute to technical limitations such as small protein sets and limited rate ranges, as well as biological factors including the multifunctional nature of viral proteins. Crucially, however, viral mimics were not enriched for positively selected genes; if anything, the fraction of such genes was lower in mimics than in other viral proteins across all four lineages. In the few mimicking–target complexes that could be modeled with high confidence, interface residues of viral mimics were more conserved than surface residues, mirroring the host-side pattern. The single positively selected residue detected in a viral mimic, asparagine 15 in the vaccinia Bcl-2-like protein OPG035, sits far from the interface with its human target, pointing away from any adaptive remodeling of the binding surface.

The overall message is a reframing of how host–virus conflict plays out at the molecular level. While arms races do occur, particularly in immune and restriction factors, the interactions mediated by mimicry appear governed by constraint rather than escalation. Viruses have exploited the host’s inability to escape: by targeting highly connected, highly expressed, functionally essential proteins through surfaces the host must preserve, mimics anchor themselves to interaction networks that evolution cannot easily redeploy. The conserved nature of these interfaces may also carry practical value, the authors suggest, since stable binding regions could serve as targets for antiviral drugs designed to disrupt mimicry-mediated interactions. And because these principles govern the conservation and evolvability of host–virus interaction networks, they may help predict which viruses can switch hosts and which barriers stand in the way of zoonotic emergence. The study’s data and code are openly available, offering a resource for the growing field of structural virology.

Subject of Research: Evolutionary dynamics of viral molecular mimicry and host protein interactions in large DNA viruses

Article Title: The evolutionary dynamics between viral mimics and host proteins

Article References: Fuchs, R., Schor, O., Naim, B., Tussia-Cohen, D., Mozzi, A., Forni, D., Friedman, S., Haggai, Z., Sironi, M., & Hagai, T. (2026). The evolutionary dynamics between viral mimics and host proteins. Molecular Systems Biology, 22(6), 902-927. https://doi.org/10.1038/s44320-026-00200-1

Image Credits: AI Generated

DOI: 10.1038/s44320-026-00200-1

Keywords: molecular mimicry, virus-host interactions, viral evolution, protein-protein interactions, AlphaFold, dN/dS, positive selection, herpesvirus, poxvirus, structural biology, host-pathogen coevolution, protein interfaces

The study, published in BMC Genomics, began with a straightforward technical goal: use high-throughput sequencing to recover complete organellar genomes from the three species, which represent an important but poorly characterized genus within the Combretaceae family. Achieving that goal proved anything but simple for the mitochondrial compartment. Whereas the chloroplast genomes assembled into the familiar quadripartite architecture seen across most flowering plants—a large single-copy region, a small single-copy region and a pair of inverted repeats—the mitochondrial genomes refused to conform to any single template. T. chebula and T. intricata each yielded a set of three circular molecules plus one linear molecule, while T. franchetii presented two linear molecules, an arrangement the authors attribute to extensive recombination events that have repeatedly reshuffled the mitochondrial DNA.

The size disparity is equally dramatic. The chloroplast genomes of the three species spanned a narrow range of just 159,700 to 159,971 base pairs and carried between 103 and 107 genes, with variations confined to specific regions. The mitochondrial genomes, by contrast, ranged from 350,904 to 365,711 base pairs—an expansion of roughly 120,000 base pairs relative to the chloroplast compartment and a degree of variation that dwarfs the differences observed in the chloroplast genomes. This pattern, in which the chloroplast genome remains remarkably conserved while the mitochondrial genome undergoes structural upheaval, mirrors what has been documented in other angiosperm lineages but is documented here in exceptional detail for Terminalia.

To probe the functional consequences of these structural differences, the researchers turned to Ka/Ks analysis—the ratio of nonsynonymous to synonymous substitution rates—which serves as a molecular detective for natural selection. Several mitochondrial genes, including rps1 and nad4, showed signatures of positive selection, suggesting that these proteins may have been recruited into adaptive roles, potentially related to the physiological demands of the species’ environments. The finding is particularly intriguing because mitochondrial genes in plants are typically regarded as evolutionarily staid, accumulating mutations slowly and with little evidence of directional pressure. The identification of positively selected sites in Terminalia hints that the organelle’s proteins may be more evolutionarily labile than conventional wisdom suggests, at least in this genus.

Equally revealing was the analysis of RNA editing, the post-transcriptional process by which specific cytidine residues in mitochondrial transcripts are converted to uridine. In all three species, the researchers found that every observed editing event was a C-to-U conversion, and that these changes systematically enhanced the hydrophobicity of the encoded proteins. This is consistent with the view that RNA editing in plant mitochondria acts as a corrective mechanism, fine-tuning protein sequences to preserve or improve the functional properties of membrane-associated enzymes in the electron transport chain. The uniformity of the C-to-U pattern across the three species suggests that this editing machinery is an ancient and deeply conserved feature of the Terminalia mitochondrial system, even as the underlying genome architecture has been repeatedly rearranged.

The contrast between the two genomes extends to their repetitive landscapes and mutational dynamics. Simple sequence repeats and longer repetitive elements, catalogued in the study’s supplementary tables, provide insight into the mechanisms generating genome size variation, particularly in the mitochondrial compartment where recombination between repeats can generate the alternative molecular conformations—circles and linear molecules—observed in the assemblies. Nucleotide diversity analysis, reported as Pi values across the organellar genomes, identified specific regions of elevated variation, offering potential molecular markers for future population genetic and phylogeographic work in the genus. Meanwhile, analysis of relative synonymous codon usage revealed patterns of codon bias that reflect the underlying mutational and selection pressures acting on each compartment.

Beyond structural characterization, the study tackled a question of broader systematic importance: where exactly does Terminalia sit in the flowering plant tree of life? Using protein-coding genes from both organellar compartments, the researchers performed maximum-likelihood phylogenetic analyses that clarified the evolutionary position of the genus within the Combretaceae and its relationships to related lineages. The inclusion of mitochondrial data proved particularly valuable, as the structural lability of plant mitochondrial genomes has historically complicated their use in phylogenetics. By demonstrating that, despite their architectural chaos, the mitochondrial genomes of these three species retain sufficient phylogenetically informative signal, the authors have bolstered the case for incorporating mitochondrial sequences into future systematic studies of Terminalia and its relatives.

One of the more fascinating aspects of plant organellar biology captured in this study is the phenomenon of mitochondrial plastid DNAs, or MTPTs—fragments of chloroplast DNA that have migrated into the mitochondrial genome over evolutionary time. Such transfers are a hallmark of endosymbiotic gene evolution and can shed light on the frequency and directionality of intercompartmental DNA exchange. Their presence and distribution in the Terminalia mitochondrial genomes provide a molecular record of past genetic conversations between the two organelles, and their characterization in this study adds to a growing body of comparative data across angiosperms. The locally collinear block analysis used to compare genome structures across species further illuminated how syntenic regions have been preserved or disrupted by recombination, painting a dynamic picture of genome evolution in motion.

The practical implications of this work reach beyond pure evolutionary biology. Terminalia species are economically and medicinally significant, particularly T. chebula, whose fruits are used in traditional medicine systems and whose genomic resources have been scarce. The complete organellar genomes now available provide a foundation for DNA barcoding, species authentication and conservation genetics in a genus where morphological identification can be challenging. The hyper-variable regions identified through nucleotide diversity analysis are likely to prove especially useful as markers for distinguishing species and tracing the geographic origins of medicinal plant material, a growing concern in the herbal products trade.

Funded by China’s National Key R&D Program, the Strategic Priority Research Program of the Chinese Academy of Sciences and the National Natural Science Foundation of China, among other sources, the study also reflects the increasing accessibility of complete organellar genome assembly as a standard tool in plant comparative genomics. What sets this contribution apart is the paired treatment of both compartments within the same three species, allowing the authors to draw direct, controlled comparisons between a genome that is structurally frozen and one that is structurally fluid. The result is a vivid illustration of the decoupled evolutionary tempos of the plant cell’s two endosymbiotic residents—and a reminder that even within a single lineage, different genomes can write very different evolutionary stories. For Terminalia, that story is only just beginning to be told.

Subject of Research: Comparative analysis of chloroplast and mitochondrial genomes in three Terminalia species

Article Title: Comparative analysis of organelle genomes in three Terminalia species reveals structure evolution and phylogenetic position

Article References: Liu, X., Zhang, Y., Luo, P., Yang, Z., Zuo, Y., Crabbe, M. J. C., Li, G., & Zhang, T. (2026). Comparative analysis of organelle genomes in three Terminalia species reveals structure evolution and phylogenetic position. BMC Genomics. https://doi.org/10.1186/s12864-026-13381-8

Image Credits: AI Generated

DOI: 10.1186/s12864-026-13381-8

Keywords: Terminalia, organelle genome, mitochondrial genome, chloroplast genome, comparative genomics, genome evolution, RNA editing, positive selection, phylogenetics, Combretaceae, recombination, molecular evolution

The research team, led by Claudia Pérez-Calles and Jingtao Lilue, with senior authors Ashlee H. Rowe and Thomas M. Keane, built the new genomes using modern long-read sequencing and assembly approaches, producing reference-quality resources for Onychomys and its non-resistant relative. This comparative framework matters because earlier work on grasshopper mice had focused largely on a single gene family: the voltage-gated sodium channels, and in particular Nav1.8, a channel expressed in pain-sensing neurons. Previous studies had shown that structural and functional modifications of Nav1.8 in grasshopper mice block the effect of the painful toxins delivered by their scorpion prey, effectively converting a weapon of deterrence into dinner. Yet important questions remained about whether other molecular systems contribute to toxin resistance, and about how the animals respond physiologically when they are actually exposed to toxins in the wild.

By scanning the newly assembled genomes for signatures of positive selection, the researchers identified Onychomys-specific mutations in another sodium channel gene, Scn3a, which encodes the Nav1.3 channel. Unlike Nav1.8, Nav1.3 is expressed in the central nervous system and in the peripheral sensory system after nerve damage, where it is associated with heightened neuronal excitability. The discovery that grasshopper mice carry their own distinctive variants of this channel suggests that toxin resistance is not the work of a single molecular tweak but of a broader rewiring of the excitability machinery of sensory and central neurons. If Nav1.8 keeps painful toxins from firing up peripheral nociceptors, the newly identified Scn3a mutations may help ensure that any signals that do get through, or that arise from tissue damage during a scorpion battle, are blunted as well. The authors are careful to frame these as candidate adaptations whose precise functional consequences will require further experimental testing, but their recurrence in a gene so central to pain signalling makes them a compelling addition to the story.

The pangenome approach also revealed something entirely unexpected outside the nervous system: an Onychomys-specific tandem duplication of a gene called Cblif, which encodes a glycoprotein crucial for the absorption of vitamin B12 in the gut. At first glance, a vitamin transport gene seems an odd companion to toxin resistance, but the researchers connect it to the grasshopper mouse’s unusual dietary and anatomical specialisation. These rodents are carnivorous in a family dominated by seed eaters, and their stomach morphology is distinctive, characterized by an abundance of parietal cells, the acid-secreting cells of the gastric lining. The study found that Cblif is expressed in these parietal cells, and the researchers propose that the gene duplication may represent an adaptation supporting the species’ meat-rich diet and its modified stomach architecture. In an animal that consumes large quantities of arthropod prey, efficient handling of nutrients and gastric chemistry could be as important to survival as venom resistance itself, and the duplication illustrates how a pangenome can surface copy-number changes that single-reference comparisons routinely miss.

To move beyond static genome comparisons and observe the molecular response to toxin exposure as it happens, the team generated RNA sequencing data from two key sensory structures: the dorsal root ganglion, which houses the cell bodies of sensory neurons that relay pain signals from the body to the spinal cord, and the trigeminal ganglion, which performs the equivalent role for the face and head. Grasshopper mice were exposed to toxic sprays from pinacate beetles, another chemically defended prey item that these rodents subdue with gusto. The transcriptomic readout revealed that in Onychomys torridus, the southern grasshopper mouse, genes associated with transportation processes were upregulated following toxin exposure. This pattern suggests that when the animals encounter defensive chemicals, they mobilize cellular transport machinery, potentially to move toxins or their metabolites away from sensitive tissues, to shuttle protective molecules to where they are needed, or to manage the cellular stress caused by chemical assault.

Taken together, the findings sketch a multi-layered model of toxin resistance in grasshopper mice. At the first layer sit the sodium channel adaptations, with Nav1.8 modifications established by earlier work and Scn3a mutations newly identified here, that alter how pain and danger signals are generated and propagated. At the second layer sits an inducible transcriptional response, in which transport-related genes are dialled up in sensory ganglia after chemical exposure, providing a dynamic defence that complements the hard-wired channel changes. And at a third layer, the Cblif duplication hints at the digestive and metabolic specialisations that accompany a predatory lifestyle, reminding readers that adaptation to toxic prey reshapes far more than the nervous system. The authors conclude that Onychomys-specific Scn3a mutations, together with the upregulation of transport-related genes following toxin exposure, may contribute to the evolution of toxin resistance in these rodents, a formulation that is deliberately measured but nonetheless expands the known genetic substrate of the trait.

The significance of the work extends beyond one charismatic genus of desert mice. Pangenomics, the practice of building reference resources that capture the full spectrum of variation within a group of related organisms, is rapidly becoming the standard for species where a single reference genome conceals important structural differences, such as duplications, inversions and gene losses. The Onychomys study demonstrates how such resources can expose candidate adaptations that would be invisible in a conventional single-genome alignment, from tandem duplications to lineage-specific amino acid changes in physiologically critical genes. It also provides a template for studying evolutionary convergence, since toxin resistance has evolved independently in several lineages that interact with venomous prey, including other rodents, hedgehogs and opossums. Comparative work across these systems, enabled by reference-quality genomes, can help distinguish shared molecular solutions from lineage-specific innovations.

There are also potential biomedical implications. Sodium channelopathies are central to chronic pain, epilepsy and cardiac arrhythmia, and the variants that grasshopper mice have evolved under natural selection represent natural experiments in how channel function can be modified without catastrophic side effects. Understanding precisely how the Onychomys Nav1.8 and Nav1.3 variants alter channel gating, drug binding and toxin sensitivity could inform the design of new analgesics that mimic the mouse’s painlessness. Similarly, the transport genes upregulated after toxin exposure may point to endogenous detoxification and cytoprotective pathways that could be pharmacologically enhanced. The researchers caution that their results are a foundation rather than a finished edifice: functional validation, including electrophysiological characterization of the mutant channels and mechanistic dissection of the transport response, remains to be done.

For now, the grasshopper mouse has yielded another instalment of its secrets, and the picture that emerges is one of layered, genome-wide specialization. High-quality reference genomes for Onychomys species and Peromyscus eremicus now stand as public resources for the community, and the specific discoveries, from Scn3a mutations to the Cblif duplication to the toxin-induced transport response, provide a rich set of hypotheses for the next generation of experiments. What was once framed as a single-gene story about a pain-proof sodium channel has become a systems-level account of how a mammalian predator co-evolves with dangerous prey, rewiring its neurons, its digestive physiology and its stress responses in the process. As the authors and their collaborators continue to probe these adaptations, the howling little hunter of the desert may yet teach medicine a thing or two about the molecular biology of pain.

Subject of Research: Genomic adaptations underlying toxin resistance in predatory grasshopper mice (Onychomys)

Article Title: The Onychomys pangenome reveals the unique molecular adaptations that confer toxin resistance

Article References: Pérez-Calles, C., Lilue, J., Anderson, E., Haggerty, L., Martin, F. J., McCarthy, S. A., Adams, D. J., Thybert, D., Rowe, A. H., & Keane, T. M. (2026). The Onychomys pangenome reveals the unique molecular adaptations that confer toxin resistance. Genome Biology. https://doi.org/10.1186/s13059-026-04288-4

Image Credits: AI Generated

DOI: 10.1186/s13059-026-04288-4

Keywords: grasshopper mouse, Onychomys, pangenome, toxin resistance, Nav1.8, Scn3a, sodium channels, Cblif, gene duplication, scorpion venom, dorsal root ganglion, positive selection

The research team, led by Siobhán McClean of University College Dublin with collaborators including Joanna Drabinska, Lucia O’Connor and Caoilin McClean, took advantage of a uniquely valuable resource: an international reference panel of 41 fully sequenced P. aeruginosa strains assembled by De Soyza and colleagues. Within that panel sit three independent series of sequential isolates, each recovered from a different person with cystic fibrosis in a geographically distinct region, and each spanning roughly seven years of infection. The German series comprises AA2, AA43 and AA44, with the latter two isolated 7.5 years after the first and shortly before the patient’s death. The Seattle series from a pediatric patient includes AMT 0060-3, recovered when the child was 7.7 years old, and two later strains isolated 7.9 years afterward. A third series, AMT0023-30 and AMT0023-34, was isolated eight years apart from a patient who was only six months old at the first sampling; the later strain carried 68 unique mutations relative to the earlier one.

Previous phenotypic work on these strains had already established a consistent pattern: reduced virulence in the Galleria mellonella acute infection model was the only trait altered in every late isolate, while pyocyanin production, the blue-green pigment that contributes to tissue damage, fell in four of the five late strains. Motility traits such as swarming and swimming also declined in most late isolates, with some functions lost entirely. What remained unknown was whether these convergent phenotypes reflected convergent molecular changes. To find out, the researchers performed label-free quantitative proteomics on all eight strains, using a Bruker TimsTOF Pro mass spectrometer coupled to an Evosep One chromatography system with PASEF acquisition, and analyzed the data in MaxQuant against the PAO1 reference proteome with a 1 percent false discovery rate.

The scale of change within each series was striking. In the AMT0060 series, 138 proteins changed abundance by at least 1.5-fold in one late strain and 166 in the other, with 57 changes shared between the two. In the AA2 series, 78 proteins changed in AA43 and 267 in AA44, though only 30 overlapped between the two late strains. The AMT0023 pair showed 182 altered proteins. Given the enormous diversity of P. aeruginosa, the team specifically searched for proteins altered in two or more independent series, reasoning that such changes would represent conserved adaptation pathways rather than patient-specific quirks.

The result was remarkable. Only 16 proteins in total were altered across all three series, and 11 of them showed a consistent direction of change: increased abundance in the late strains of every series. In nearly every case, these proteins were undetectable in the early isolates, meaning the underlying genes had been switched on during years of colonization. The probability that the same three proteins, PA2572, PA3819 and PA5028, would show increased abundance in all five late strains from three independent early ancestors by chance alone was calculated at 5.06 × 10⁻⁵³, which the authors describe as very strong evidence of positive selection. Even for the eight proteins that appeared in only one late isolate per patient, the probability of such a pattern arising randomly in a genome of roughly 5,570 open reading frames was 1.6 × 10⁻¹⁹.

The identities of these 11 proteins tell a coherent evolutionary story. PA3819 is an outer membrane lipoprotein with a glycine zipper domain, encoded within the AlgU regulon that governs alginate production and membrane stress responses, and previously linked to Toll-like receptor signaling in mucoid strains. PA2572 is an HD-GYP domain two-component response regulator sitting beside a chemotaxis transducer gene; it binds the sensor PA2573, influences ExoS and pyocyanin production, dampens swarming motility, and does not hydrolyze c-di-GMP unlike its two paralogs. PA3702, better known as WspR, is the diguanylate cyclase response regulator of the Wsp surface-sensing system, which responds to cell envelope stress, suppresses flagellar motility and promotes biofilm formation, consistent with the loss of motility widely reported for chronic isolates. PA5028 and PA1462 are cytoplasmic membrane proteins of the ParAB family, partners of the DNA-binding partitioning protein ParB, whose systems regulate cell division and act as global regulators of multiple proteins. CifR, a TetR-family epoxide-responsive repressor controlling the CFTR inhibitory factor Cif, rose 10- to 11-fold in one late isolate of each series, matching earlier observations that CF isolates maintain CifR expression over time. The set is rounded out by PA2551, a probable LysR-family transcriptional regulator that may counteract stress-induced growth slowdown; PA2679, a methyltransferase whose expression rises under hypoxia; PA2883, a membrane protein co-expressed with the c-di-GMP-binding protein MapZ and strongly induced by airway epithelia; PA3084, a hypothetical protein identified as conditionally essential for cardiomyocyte infection; and PA3271, a two-component sensor kinase whose disruption alters virulence genes including pyochelin synthesis, elastase and flagellar proteins.

Notably absent from this list are antibiotic resistance mechanisms, even though several resistance-associated proteins, such as the MexA efflux component, rose dramatically in some late strains. The authors suggest that differing antibiotic regimens among the three patients may explain the lack of a conserved resistance signature. Convergence was also evident at the pathway level rather than the individual protein level: virulence-associated secretion systems and secreted factors declined across multiple strains, and phenazine biosynthesis enzymes such as PhzB, PhzF and PhzG dropped in the AA2 and AMT0023 series but not in AMT0060, indicating that reduced pyocyanin production can arise through multiple regulatory routes, including quorum sensing and quinolone signaling, where LasR and PQS-associated proteins were also reduced.

To test whether the upregulated proteins actually confer a functional advantage, the team compared gene-deletion mutants of PA2572 and PA3819 with the wild-type MPAO1 strain under stresses that mimic the cystic fibrosis lung. Under normal conditions the mutants grew identically to the wild type, with comparable growth kinetics and stationary-phase densities. But the ΔPA3819 mutant showed clearly impaired survival under oxidative stress from 1 mM hydrogen peroxide, and both mutants fared worse under osmotic stress from 0.5 M sodium chloride and elevated temperature of 45°C. Antibiotic susceptibility testing added a further twist: loss of PA2572 increased susceptibility to imipenem, aztreonam and norfloxacin, while loss of PA3819 increased susceptibility to aztreonam alone. Together, these results suggest that the elevated abundance of these proteins in late isolates directly supports bacterial fitness under chronic-infection conditions and may contribute to the enhanced antibiotic resistance that emerges over years of treatment.

Intriguingly, quantitative PCR showed that the increased protein abundance was not mirrored at the transcript level. Expression of PA3819 was actually repressed 3.5-fold in two late strains, and PA2572 was repressed 5-fold in AA44, pointing to translational or post-translational control. Searching the amino acid sequences of the three consistently upregulated proteins revealed multiple predicted phosphorylation, glycosylation and N-myristoylation sites associated with protein stability, and a shared conserved motif resembling tyrosine phosphorylation sites found in bacterial effectors such as Tir of enteropathogenic Escherichia coli and Tarp of Chlamydia trachomatis. Tyrosine phosphorylation is known to regulate bacterial virulence traits, and the authors propose that such modifications may stabilize these proteins during chronic infection. Because earlier comparative studies of sequential isolates relied on less sensitive methods such as two-dimensional electrophoresis, none of these 11 proteins had previously been flagged as consistently increased, underscoring the power of modern high-throughput proteomics. Each of the 11 proteins, the authors conclude, represents a potential target for adjuvant therapies designed to disable the adaptation process itself and prevent acute infection from hardening into lifelong chronic colonization.

Subject of Research: Proteomic analysis of sequential Pseudomonas aeruginosa strains from cystic fibrosis patients to identify proteins under positive selection during chronic infection

Article Title: Proteomic Analysis of Three Independent Series of Sequential Cystic Fibrosis Strains in an International Pseudomonas aeruginosa Reference Panel Indicates Positive Selection in Late Infection Strains

Article References: Drabinska, J., O'Connor, L., McClean, C., & McClean, S. (2026). Proteomic Analysis of Three Independent Series of Sequential Cystic Fibrosis Strains in an International Pseudomonas aeruginosa Reference Panel Indicates Positive Selection in Late Infection Strains. MicrobiologyOpen, 15(5), Article e70417. https://doi.org/10.1002/mbo3.70417

Image Credits: AI Generated

DOI: 10.1002/mbo3.70417

Keywords: Pseudomonas aeruginosa, cystic fibrosis, proteomics, chronic infection, positive selection, bacterial adaptation, virulence, two-component regulators, antibiotic resistance, WspR, hypoxia response, host adaptation

The research team, led by scientists at Northwest A&F University in Yangling, China, sequenced the whole genomes of 65 wine-related H. uvarum strains isolated from major wine-producing regions of northwestern China, including Shaanxi, Ningxia, Gansu, and Xinjiang. These newly generated sequences were combined with 86 publicly available genome datasets, yielding a total of 151 strains for population genomic analysis, with samples drawn from China, Australia, Europe, the United States, and other locations. The newly sequenced strains showed exceptionally deep sequencing coverage, ranging from roughly 726-fold to more than 1,500-fold, ensuring high confidence in the variants detected.

From the combined dataset, the researchers identified 575,222 high-quality genetic variants, including more than half a million single nucleotide polymorphisms, after masking repetitive and low-complexity regions of the reference genome. Downstream analyses focused on 483,564 biallelic SNPs. Three independent approaches—phylogenetic tree construction, ancestry coefficient estimation, and principal component analysis—told a consistent story: strains sampled in China are broadly distinguishable from those sampled on other continents, confirming that geographic isolation has played a major role in shaping intercontinental population divergence in this species.

Yet the picture is far more tangled than a simple tale of isolated populations drifting apart. Using the TreeMix software to model migration between clades, the team detected substantial gene flow between geographically paired clades after their divergence. In the optimal model, gene flow was inferred from a Chinese clade to an Australian clade, from another Chinese clade to a European clade, and from the European clade back to a third Chinese clade. The f-branch statistic, a method that detects excess allele sharing between paired lineages, corroborated these signals: the highest intercontinental value, 49.84 percent, linked a Chinese clade with an Australian clade, with additional elevated values connecting Chinese, European, and Australian lineages. Together, these results point to ongoing intercontinental dispersal of H. uvarum, likely facilitated by human activity or insect vectors, a pattern reminiscent of what has been documented in the better-known wine yeast Saccharomyces cerevisiae.

Beyond connectivity, the study revealed that local environments have left distinct evolutionary fingerprints on different populations. Scanning for selective sweeps with the RAiSD tool, the researchers identified 117 candidate genes under positive selection in strains from Ningxia, China, and 141 in Australian strains, with only 23 genes shared between the two sets. These positively selected regions showed significantly elevated genetic differentiation and reduced diversity compared to the genomic background—classic hallmarks of recent adaptation. The Ningxia genes were significantly enriched for Gene Ontology terms related to the positive regulation of filamentous growth in response to external stimuli, such as starvation, pH stress, and biotic stimulus. The authors suggest these adaptations may help Ningxia strains colonize fruit surfaces, echoing earlier proposals that the yeast’s ability to form pseudohyphae in rich media confers an advantage for fruit colonization.

Intriguingly, the stress-related GO term “cytoplasmic stress granule” was significantly enriched among positively selected genes in both the Ningxia and Australian subsets, but the two regions shared only two of the six stress granule-associated genes in each set. Stress granules are cytoplasmic assemblies that sequester inactive messenger RNAs under conditions such as heat shock, oxidative stress, and nutrient deprivation, allowing cells to preferentially translate stress-response proteins. The fact that different genes underpin this same function in the two regions suggests that Ningxia and Australian populations have faced distinct environmental pressures and have evolved different molecular solutions to cope with stress.

The study also touched on one of the most curious features of the genus Hanseniaspora: its extensive loss of DNA repair genes. Previous work showed that the Faster-Evolving Lineage, to which H. uvarum belongs, lost dozens of genes involved in cell-cycle control and DNA repair, and also evolved a novel cis-regulatory mode for its core histone genes. Despite this genetic erosion, the new analysis found that DNA repair terms showed marginal enrichment among positively selected genes in the Ningxia subset, and that two classes of histone acetyltransferase complexes involved in DNA repair—the NuA4 complex and the SAGA and SLIK complexes—were significantly or marginally enriched in both regional subsets. Moreover, the pangenome analysis revealed that a subset of strains may carry DNA repair complex genes not present in the rest of the species, hinting that some populations have partially compensated for ancient gene losses through acquired or retained genetic material.

To capture the full gene repertoire of the species, the team constructed a pangenome from 159 strains, including eight additional genome assemblies. They identified 4,991 gene families, of which 3,340 were present in all strains (the core), while the remainder were divided into soft-core, shell, cloud, and private categories. Perhaps the most striking result came from Heaps’ Law analysis: with a decay parameter of 0.51—well below the threshold of 1—the H. uvarum pangenome is open, meaning new gene families keep appearing as more genomes are sampled. This is notable because the sampling focused almost entirely on anthropogenic environments such as vineyards and wineries, a relatively homogeneous niche. An earlier pangenome analysis based on just eight strains had concluded the pangenome was closed; the new, much larger dataset overturns that view and suggests the species harbors substantial adaptive potential for diverse stresses.

The practical implications reach well beyond evolutionary theory. H. uvarum is valued in winemaking for its ability to increase esters and volatile phenols, reduce volatile acidity, and improve the sensory profile of wine when used in co-fermentation with Saccharomyces cerevisiae. It also participates in fermentations of cider, cocoa, coffee, and pineapple wine, and related species serve as biocontrol agents against postharvest fruit diseases. A genomic understanding of how regional populations differ—in stress tolerance, filamentous growth, and metabolic capacity—could guide the selection of indigenous starter strains tailored to specific terroirs and fermentation goals, including recent efforts to screen Chinese Hanseniaspora strains for ethanol reduction in wine.

The authors caution that their sampling, while broad, remains uneven: wild-niche strains were absent because genomic data were not publicly available, and Chinese sampling was concentrated in Ningxia and Shaanxi. Future studies incorporating strains from more diverse ecological niches, broader geographic regions, and longer time spans will be needed to refine the evolutionary picture. Nevertheless, by combining deep whole-genome sequencing, phylogenetics, admixture modeling, selective sweep detection, and pangenomics, the study delivers high-quality genomic resources and a foundational framework for population genomics of non-Saccharomyces yeasts—a field long overshadowed by work on Saccharomyces cerevisiae. For a species once considered merely a fleeting early fermenter, Hanseniaspora uvarum is proving to be a genetically rich, globally connected, and remarkably adaptable microbe whose evolutionary story is only beginning to unfold.

Subject of Research: Population genomics, gene flow, and positive selection in the wine-related yeast Hanseniaspora uvarum

Article Title: Population genomics reveals gene flow and positive selection patterns in the wine-related yeast Hanseniaspora uvarum

Article References: Ma, R., Wang, H., Wei, Y., Sun, Y., Xue, J., Qin, Y., Tao, S., & Liu, Y. (2026). Population genomics reveals gene flow and positive selection patterns in the wine-related yeast Hanseniaspora uvarum. Stress Biology, 6(1), Article 54. https://doi.org/10.1007/s44154-026-00319-z

Image Credits: AI Generated

DOI: 10.1007/s44154-026-00319-z

Keywords: Hanseniaspora uvarum, non-Saccharomyces yeasts, population genomics, gene flow, introgression, positive selection, pangenome, wine fermentation, selective sweep, stress granules, DNA repair, geographic divergence