An international consortium of researchers generated an extraordinary trove of data: 771 multiomics datasets spanning embryonic development and adult tissues in Atlantic salmon and rainbow trout, totalling 77.7 billion read pairs. The work was carried out under the European AQUA-FAANG project, part of the Functional Annotation of Animal Genomes initiative, and combined RNA sequencing to measure gene expression with ATAC-seq and ChIP-seq to map open chromatin and epigenetic marks. From these data, the team identified 319,718 robust open chromatin regions in salmon and 194,002 in trout, and used a computational approach called ChromHMM to classify the genome into functional states, pinpointing tens of thousands of active promoters and enhancers in each species.

The reason salmonids are so valuable for this kind of work lies in their peculiar genomic history. Roughly 80 to 100 million years ago, the ancestor of all salmon and trout experienced a whole genome duplication, an autotetraploidization event that doubled the entire genome within a single species. Unlike the ancient duplications that shaped all vertebrates more than half a billion years ago, this salmonid event is recent enough that the genome is still in the midst of rediploidization, the slow return to normal diploid inheritance. Around half of salmonid genes are still retained as functional duplicate pairs, known as ohnologues, sitting in large collinear blocks on duplicated chromosomes.

Crucially, rediploidization did not happen uniformly across the genome. Some duplicated regions resolved back into diploid inheritance before salmon and trout lineages split roughly 25 million years ago, giving their genes a long head start on divergence. Other regions resolved independently in each species, meaning their duplicate pairs are evolutionarily much younger. This stratification, called asynchronous rediploidization, allowed the researchers to compare duplicate genes at different stages of post-duplication evolution within the same genomes, effectively providing a series of snapshots of the same evolutionary process at different ages.

The central finding is striking: the pace of regulatory evolution after genome duplication is not random but is governed by the same developmental constraints that shape gene evolution across all vertebrates. Measuring expression divergence between duplicate pairs using Jensen-Shannon distance, the team found that divergence was highest in early embryos, before the maternal-to-zygotic transition, and fell steadily through embryogenesis, reaching its minimum at the pharyngula stage, which corresponds to the vertebrate phylotypic period. This is the stage, long recognized in evolutionary developmental biology, when embryos of different species look most alike and when pleiotropic genes are recruited across many developing tissues, creating a densely interconnected regulatory environment that resists change.

The correlation was remarkably tight. The pattern of decreasing expression divergence across embryogenesis was nearly identical between early and late rediploidization pairs, with a Pearson correlation of 0.97, and it also matched the divergence of orthologous genes between salmon and trout. In other words, the constraints acting on duplicate genes within a single genome mirror those acting on the same genes across species. The authors argue that these pleiotropic constraints do not merely limit divergence after duplication; they actively drive which duplicates are retained, because genes expressed during mid-to-late segmentation tend to be dosage-sensitive, and keeping both copies of such genes buffers against harmful imbalances in gene dose.

Adult tissues told a different and equally revealing story. Expression divergence between duplicates varied enormously across the body, with the brain showing the lowest divergence, consistent with its status as the tissue under the strongest purifying selection, while liver, ovary and testis showed the highest. Sexual maturation had little effect in most tissues, but mature testis displayed elevated divergence compared with immature testis. When the researchers compared orthologous genes between salmon and trout, they found that duplicates retained from the genome duplication had evolved more slowly than single-copy genes in gill, head kidney and distal intestine, though in the brain even single-copy genes evolved slowly, and in the ovary, maturation stage mattered more than duplication status.

Turning from genes to their regulatory elements, the team classified every active promoter and enhancer according to its fate after duplication: shared, meaning both duplicated copies remained active; alignable only, meaning the sequence was conserved but activity was lost from one copy; or exclusive, meaning the active element existed on only one chromosome. Promoters proved conservative, with 53.5 percent shared, closely matching the estimated 55 percent retention rate of duplicate gene pairs. Enhancers were far more dynamic, with only 33.3 percent shared and 43.8 percent falling into the alignable-only category, confirming that enhancers turn over faster than promoters after genome duplication, a pattern also seen when comparing regulatory elements across species.

The link between enhancer fate and gene divergence was direct. Duplicate gene pairs whose expression remained conserved had significantly more shared enhancers, while pairs with diverged expression had more exclusive enhancers, and their enhancer-usage profiles across tissues were measurably farther apart. In adult tissues, enhancer-usage distance tracked expression distance closely, whereas during embryogenesis it did not, suggesting that promoter changes and a specific subset of shared enhancers dominate regulatory divergence in embryos, while wholesale remodelling of the enhancer repertoire drives divergence in adult organs. Transposable elements added another layer: exclusive enhancers overlapped transposon sequences more than twice as often as shared enhancers, and DNA transposons of the TcMar class, the most active group in the salmon genome, were specifically enriched in enhancers of diverged duplicate pairs, implicating these jumping genes both in disabling old enhancers and in creating new ones.

Perhaps the most evocative result concerns conserved non-coding elements, ancient DNA sequences under purifying selection across hundreds of millions of years of vertebrate evolution. Among 24,007 enhancer-associated conserved elements in salmon, 61.4 percent were retained as shared duplicate pairs, and these were strongly enriched for the oldest categories, dating back to the ancestor of all bony vertebrates. The shared elements active during late somitogenesis, the phylotypic period, were packed with motifs for master developmental transcription factors such as POU5F1, Sox and Pax family proteins, precisely the regulators that orchestrate embryonic patterning. This suggests that duplicated enhancers carrying deeply conserved developmental instructions are functionally retained in duplicate, reinforcing the developmental lock that limits evolutionary change at the hourglass waist. The study, whose data are openly available through the FAANG portal and SalmoBase, not only illuminates how genomes recover from duplication but also provides a resource for breeding improved aquaculture strains and for conserving wild salmonid populations whose genomes carry this extraordinary evolutionary archive.

Subject of Research: Gene-regulatory evolution following whole genome duplication in salmonid fishes

Article Title: Developmental contexts of gene-regulatory evolution following whole genome duplication in salmonids

Article References: Baudement, M.-O., Morata, D. P., Gillard, G. B., Dewari, P. S., Gundappa, M. K., Podgorniak, T., Grønvold, L., Baranasic, D., Laurent, A., Giudicelli, F., Zunar, B., Carrera-García, E., Perquis, A., Brionne, A., Thi Nguyen, T., Ruiz Daniels, R., Merino, G. A., Thybert, D., Ilsley, G. R., … Macqueen, D. J. (2026). Developmental contexts of gene-regulatory evolution following whole genome duplication in salmonids. Nature Ecology & Evolution, 10(10), 1959-1981. https://doi.org/10.1038/s41559-026-03171-6

Image Credits: AI Generated

DOI: 10.1038/s41559-026-03171-6

Keywords: whole genome duplication, salmonids, Atlantic salmon, rainbow trout, ohnologues, rediploidization, enhancers, gene regulation, phylotypic period, transposable elements, conserved non-coding elements, comparative genomics

A new study led by Academician Fuwen Wei at the Institute of Zoology, Chinese Academy of Sciences, and published in Science China Life Sciences, tackles that question head-on with a genome-scale comparison of independently evolved gliding mammals. The team generated chromosome-level reference genomes for two iconic gliders, the red-and-white giant flying squirrel (Petaurista alborufus) and the sugar glider (Petaurus breviceps), and then compared these with genomes from 17 mammalian species in total, spanning three lineages in which gliding evolved independently. The central finding is striking: the different gliding lineages almost never share the same rapidly evolving regulatory regions of DNA. Yet the genes and developmental pathways connected to those distinct regions converge on strikingly similar functions, from limb and membrane development to muscle formation and Wnt signaling. In other words, evolution reached the same destination by different roads.

The technical heart of the study lies in a class of genomic features known as conserved non-coding elements, or CNEs. These are stretches of DNA that do not encode proteins but have remained remarkably unchanged over deep evolutionary time, a pattern that usually signals an essential role in regulating gene expression. Because regulatory changes are widely believed to underpin many morphological innovations, CNEs are a natural place to look for the genetic basis of a new body plan. The researchers scanned these elements across their species panel and flagged those that showed accelerated evolution specifically in gliding lineages, defining them as gliding-specific accelerated conserved non-coding elements, or GACNEs. Acceleration in an otherwise conserved element is a classic signature of recent adaptive change, suggesting that the region may have acquired a modified regulatory function in the lineage where it evolved fastest.

When the team mapped the GACNEs onto the genomes of the three gliding lineages, the results were unambiguous. The accelerated elements were widely scattered, and the overlap between lineages was minimal. The same regulatory regions were generally not altered again and again across the independent origins of gliding. This runs counter to a simple model of convergent evolution in which the same molecular targets are hit repeatedly. Instead, it points to a more flexible architecture of adaptation, in which many different regulatory elements, distributed across the genome, can be recruited into the service of building a similar trait. For a complex structure like the patagium, which involves coordinated changes to skin, limbs, muscles, and possibly even sensory and circadian systems, there may simply be many genetic routes to the same functional endpoint.

If the specific regulatory regions differ, do the genes they influence differ too? The answer, according to the study, is subtle. The particular genes associated with GACNEs were not identical across the gliding lineages, but when the researchers performed functional enrichment analysis, a statistical test of what biological processes a set of genes participates in, the associated functions converged. Genes near the accelerated elements in each lineage were enriched for roles in appendage development, brain development, and the Wnt signaling pathway, a fundamental developmental cascade that patterns embryonic tissues and is central to limb formation. This is the crux of what the authors call regulatory convergence: different pieces of DNA, altered in different lineages, feed into overlapping gene networks and developmental programs, producing similar biological outcomes despite sequence-level divergence.

The study also revealed that GACNEs are not sprinkled randomly across the genome. Instead, they cluster into distinct evolutionary hotspots, genomic neighborhoods where accelerated regulatory elements accumulate. These hotspots occupied different locations in each of the three gliding lineages, but the genes linked to the hotspots once again showed similar functional profiles. Critically, closely related non-gliding species did not display comparable patterns of clustered acceleration, which strengthens the case that these regulatory changes are connected to gliding itself rather than to shared ancestry or general rodent- or marsupial-specific evolution. The hotspot structure suggests that gliding adaptation may involve coordinated regulatory rewiring within particular genomic regions, even when the identity of those regions varies from lineage to lineage.

To move from correlation toward mechanism, the researchers combined three lines of evidence: the genes associated with GACNEs, the genes linked to the evolutionary hotspots, and the transcription factors whose binding motifs are enriched in the accelerated elements. Transcription factors are proteins that bind regulatory DNA and switch genes on or off, so identifying which ones can interact with the accelerated regions offers a window into how those regions might act. This integrative analysis surfaced several candidate regulators of gliding adaptation, including EMX2, ZFHX3, TCF7L2, TLE1, and CTBP2. Some of these names carry real developmental weight. EMX2, for example, has previously been shown to play an important role in wing membrane formation, lending immediate biological plausibility to the candidate list.

Among the newly highlighted candidates, ZFHX3 stands out as a particularly intriguing target for future work. The study suggests it may be involved in several processes relevant to the gliding body plan, including wing membrane development, muscle formation, cartilage development, and circadian regulation. That combination is notable because a functioning glider needs more than just a sheet of skin; it requires strengthened limb bones, remodeled musculature to hold the patagium taut during flight, and, some researchers argue, appropriate timing of activity to match the demands of a nocturnal, aerodynamic lifestyle. A single regulatory hub touching multiple aspects of the phenotype could help explain how a complex adaptive trait is assembled in a coordinated fashion, and ZFHX3 now becomes a priority for experimental validation.

The team did not stop at comparative genomics. They also compared their candidate regulatory regions against previously reported enhancers, the short DNA segments that boost gene transcription in specific tissues. Several of the candidate enhancers associated with gliding overlapped with regulatory regions already known to be active in embryonic forelimb and lateral body tissue, precisely the anatomical territories from which the patagium develops. This overlap provides independent, functional support for the idea that the accelerated elements identified in gliding lineages are not genomic noise but genuine participants in the developmental program that builds the gliding apparatus. It is exactly the kind of cross-validation, linking sequence acceleration to known embryonic expression domains, that gives comparative genomics its explanatory power.

Taken together, the findings reframe how scientists think about repeated evolution. Complex adaptive traits such as gliding do not require evolution to replay the same genetic changes in every lineage. Different regulatory regions, altered independently, can converge on similar genes, networks, and developmental pathways, generating functional similarity from divergent DNA. The regulatory regions and transcription factors identified here remain candidates, and the authors are careful to note that further work combining genomic, epigenomic, and gene expression data with experimental approaches will be needed to establish exactly how these elements influence development. Even so, the study offers a framework that extends well beyond gliding mammals. For any trait that has evolved independently in multiple species, from echolocation to venom, comparing genetic changes across lineages can now reveal when evolution repeatedly tinker with the same molecular machinery, and when it takes entirely different routes to the same biological destination. In the case of gliding, at least, nature has proven itself a resourceful engineer, solving the same problem many times with many different tools.

Subject of Research: Convergent evolution of gliding in mammals through distinct regulatory genomic changes

Article Title: Different DNA, similar functions: Regulatory convergence in gliding mammals

Article References: Different DNA, similar functions: Regulatory convergence in gliding mammals. (n.d.). Original publication

Image Credits: AI Generated

DOI: Not provided

Keywords: convergent evolution, gliding mammals, conserved non-coding elements, regulatory evolution, patagium, genomics, flying squirrels, sugar glider, Wnt signaling, transcription factors, developmental biology, evolutionary genetics