Peter H. Sudmant

Understanding how habitat and life history traits contribute to population genetic structure is critical for evaluating conservation risks and identifying optimal management of wild populations. Species derived from adaptive radiations can provide a useful model for studying such patterns because the presence of some consistent traits allows for closer examination of attributes which differ. Here, we examine population structure in rockfishes (genera Sebastes and Sebastolobus ), a group of speciose, recently diverged marine fishes that exhibit a continuum of genetic structure, from cryptic species to putative genetic panmixia. In this study, we analyse low‐coverage whole genome resequencing data from nine rockfish species and identify four major types of genetic differentiation: cryptic diversity, isolation‐by‐distance (IBD), no detectable structure (putative panmixia) and no detectable structure with a single genomic region putatively underlying local adaptation. Two species, Dark ( Sebastes ciliatus ) and Northern ( S. polyspinis ) rockfishes, each exhibited cryptic diversity consisting of two sympatric groups differentiated at every chromosome throughout the genome. Black rockfish in Southeast Alaska also had two genetic groups, despite an overall signal of IBD from the West Coast of North America through the Gulf of Alaska (GOA). Five species showed evidence of genetic panmixia throughout the sampled range, while Yelloweye Rockfish exhibited high gene flow across ~4000 km, from southern California to the GOA, but had strong differentiation between the Salish Sea and the outer coast. Of the species in which no structure was detected, only Blackspotted Rockfish had one outlier region exhibiting signatures of potential local adaptation. Our results highlight how multiple mechanisms likely promote genetic structure in rockfishes, hinting at tentative links to depth distributions and offshore habitats that might influence patterns of differentiation in rockfishes more broadly. Further, this study provides genetic data for some of the most abundant rockfishes in commercial fisheries in the Northeast Pacific, enhancing the scientific information available for informing fisheries management.

Understanding the genetic architecture of pathogen resistance and its relationship to host life‐history traits is a fundamental problem in evolutionary biology, yet the conditions under which resistance costs manifest as detectable trade‐offs remain poorly understood. Here, we examine resistance in Plodia interpunctella (Indian meal moth) to its granulovirus (PiGV) across 12 inbred lines maintained without deliberate pathogen exposure, alongside an independently assembled outbred stock population as a genomic reference. We quantify resistance using LD50 values from dose–response assays, summarize developmental life‐history variation using a composite principal‐component axis derived from pupal weight, development time and growth rate, and evaluate genomic structure and window‐level associations with resistance. Resistance varied approximately two‐fold across inbred lines. Neither the composite life‐history axis nor any individual life‐history trait was significantly correlated with LD50. In contrast, genomic PC1, the primary axis of CDS‐restricted genomic differentiation, was significantly associated with resistance ( r = −0.65, p = 0.022), whereas overall pairwise distance was not. No individual PCA‐LD50 window survived multiple‐testing correction; instead, resistance‐associated signal was distributed broadly across the genome, and convergent signal spanning five chromosomes showed no enrichment for genes with known immune functions. This pattern is consistent with a diffuse, potentially polygenic basis for resistance, although the modest number of lines limits locus‐level inference. Together with prior work demonstrating resistance‐growth trade‐offs in this system, our results suggest that resistance can be genomically structured without detectable coupling to the developmental life‐history variation measured here, and that expression of resistance costs depends on genetic and environmental context.

Novel pathogens have become a major challenge faced by wildlife in the Anthropocene. White‐nose syndrome (WNS) has decimated bat populations across North America over the last two decades. Demographic and physiological evidence of adaptation in one heavily affected species, Myotis lucifugus , has prompted multiple attempts to delineate the genomic underpinnings, but these studies show little congruence in their findings. This may be due, in part, to the limitations of the genomic resources utilized and/or analytical approaches employed. Here, we performed high‐coverage whole‐genome resequencing of M. lucifugus sampled prior to ( n = 29), and 10 years after the local arrival of WNS ( n = 30), aligned to a new reference genome to identify signatures of selection associated with adaptive responses. Using 41.9 million SNPs, we implemented a combination of hard and soft sweep detection analyses, leading to the discovery of 382 genes with robust evidence of selection. Of these, 202 (49.9%) were associated with enriched gene ontology (GO) terms, many of which were tied to neuron development, organization and function. Further, approximately half (107) of genes associated with enriched GO terms interact with genes identified by previous studies. Our findings suggest reduced susceptibility to WNS is mediated through highly complex, polygenic mechanisms. Further, we demonstrate there are far more connections among WNS selection study results than previously recognized. We believe that the methods employed by our study illustrate a need for a paradigm shift in non‐model selection studies and further highlight the value of genomics as a tool for conservation management.

Bats are extraordinary among mammals, having uniquely evolved powered flight and laryngeal echolocation, along with disease resistance, extended healthspans and the ability to hibernate ¹ . However, the evolutionary history of bats and the understanding of these adaptations remain unresolved. We analysed chromosome-level, long-read genome assemblies from 103 bat species, including 42 new assemblies, representing all 21 bat families. This dataset, expanded in scope and assembly quality, yielded a new bat phylogeny. We placed Myzopodidae as the earliest branch within Vespertilionoidea, and resolved yangochiropteran relationships, identifying Emballonuroidea and Vespertilionoidea as sister groups. Our analysis revealed a mosaic evolutionary history across bats and explained why previous phylogenetic studies were misled. Chromosomal ancestral-state reconstructions supported 26 ancestral bat chromosomes. We integrated a morphological dataset of 699 characters for 65 species, including 44 pre-Quaternary fossils and representatives of most living bat families, with neutrally evolving genomic sites. Fossilized birth–death and dispersal–extinction cladogenesis analyses showed that bats, and thus powered flight, probably originated in Europe in the late Palaeocene, refuting African and North American origins. Placement of the fossil † Vielasia in the oldest ‘Eochiroptera’ clade indicates that laryngeal echolocation predates crown-bat diversification. Total evidence dating, including the fossil taxa, significantly reduced unrepresented basal branch lengths compared with molecular-only divergence estimates. By integrating comprehensive genomic and morphological datasets, analysed using innovative methods, we resolve long-standing controversies in bat biology and provide new insights into the evolutionary history and trait diversification of bats.

Of the two lineages of lentivirus that endemically infect chimpanzees, only one has served as a source of infections in hu-mans. Using HIV-CRISPR screening, we identify factors that limit the replication of lentivirus from Eastern chimpanzees. We find that CypA restricts nonzoonotic Eastern chimpanzee lentivirus due to a unique feature encoded in capsid. The ability of CypA to restrict lentivirus replication is surprising given that CypA is a host factor exploited by HIV to promote its replica-tion. The selective ability of CypA to restrict this virus provides a molecular explanation as to why lentivirus from Eastern Chimpanzees has never been observed to infect humans. Our work has important implications for understanding the origins of HIV-1 and the potential for novel zoonosis of primate lentiviruses.

Genomic methods have shown that admixture and introgression are common across animal taxa. Pacific rockfishes, genus Sebastes , are a group of commercially important species that primarily inhabit inshore, shelf and slope habitats along the North American west coast. Among these, Copper and Quillback Rockfishes are closely related species known to hybridize, particularly within the Salish Sea in North America's Pacific Northwest. Here, we investigate genetic population structure and introgression patterns in Copper and Quillback Rockfish from Alaska to California. Using whole‐genome resequencing across a broad geographic range, we seek to (1) compare population structure between these species, and (2) assess how introgression affects population structure patterns. Our analyses reveal that Copper exhibits much higher levels of population differentiation compared to Quillback, especially separating Salish Sea samples from all other populations. In contrast, Quillback populations appear to be nearly panmictic, with lower overall differentiation. Surprisingly, we detected signatures of introgression from seven other rockfish species in Copper and 10 species in Quillback. This introgression was highly regional, suggesting hybridization depended on geographic or environmental context. Yelloweye Rockfish introgression in the Salish Sea drives the strongest signal of regional population structure in Quillback. These findings provide novel insights into the range‐wide genetic structure of these species and highlight that hybridization in Sebastes is phylogenetically broader than previously appreciated.

The genus Myotis is one of the largest clades of bats, and it exhibits some of the most extreme variation in lifespans among mammals, alongside unique adaptations to viral tolerance and immune defence ^1–3 . Here, to study the evolution of these phenotypes, we generated cell lines and near-complete genome assemblies for eight closely related Myotis species. Using genome-wide screens of positive selection, analyses of structural variation and functional experiments in primary cells, we identify patterns of adaptation contributing to longevity, cancer resistance and viral interactions. We demonstrate distinct modes of adaptation to DNA and RNA viruses compared with all other mammals, with bats exhibiting genome-wide over-representation of positive selection for DNA-virus-interacting proteins and elevated rates of copy-number variation for RNA-virus-interacting proteins. Characterization of Myotis -specific duplications of the key immune factor EIF2AK2 (also known as PKR ) reveals multiple ancient segregating trans-species copy-number polymorphisms. We show that the recurrent evolution of longevity seen in Myotis is associated with positive selection in cancer pathways, and demonstrate a unique response to DNA damage in primary cells of the long-lived Myotis lucifugus . Together, our results suggest that bats’ remarkable longevity and immunity are linked through pleiotropic adaptations to viruses and ageing-related disease.

Meiotic recombination is a fundamental process that generates genetic diversity by creating new combinations of existing alleles ¹ . Whereas crossovers in humans are well characterized ² , the more frequent non-crossovers that lead to gene conversion remain challenging to study. Here we show that single high-fidelity long sequencing reads from sperm can capture both crossovers and non-crossovers, which enables effectively arbitrary sample sizes for analysis from a single male. We analysed 2,382 candidate non-crossovers in 15 sperm samples from 13 donors, and identified a consistent component with properties distinct from PRDM9-induced recombination. This phenomenon was not associated with meiotic double-strand break sites identified by DMC1 binding, the crossover recombination map or GC-biased gene conversion, but was associated with genomic fragile sites. This component is also seen in paternal non-crossover gene conversions in pedigree data ³ . Applying the same analysis to 12 blood samples ⁴ , we observed non-crossover gene conversions with similar properties, but very few crossover events. Further, we demonstrate variation between donors for the different types of recombination, even when they share the same PRDM9 genotype. We suggest that a substantial fraction of the non-crossover gene conversion events seen in sperm arise prior to meiosis.

Structural variants (SVs) contribute substantially to genetic variation and play vital roles in adaptation and disease ^1,2 . Nonetheless, SVs are poorly captured by short reads and thus remain understudied, especially in non-model organisms ^3,4 . Here, using haplotype-resolved genome assemblies from >600 vertebrate species, we comprehensively survey the landscape of SVs across >500 million years of evolution. We identify 35.3 million SVs and 3.12 billion single nucleotide variants (SNVs) segregating between two representative haplotypes across species, with SVs impacting ∼12-fold more base pairs. SV and SNV heterozygosity are correlated across species, with endangered and threatened species exhibiting reduced genetic diversity. However, the contribution of SVs relative to SNVs fundamentally differs across major vertebrate clades: given the same number of SNVs, fishes, amphibians, and reptiles have 4.3-to-9.1 times the number of SVs than birds, and 1.7-to-3.6 times more than mammals. This reduction in the relative contribution of SVs in mammals and birds is linked to fewer non-repeat-associated SVs as well as lower transposable element (TE) abundance and diversity. We identify features underlying genomic instability across vertebrates, finding that SVs frequently occur in repetitive and SNV-rich regions and are mediated by both homology and non-canonical DNA structures. Notably, G-quadruplex structures are enriched 11.5-fold around SV breakpoints in birds, while Z-DNA structures are enriched 2.2-fold in cartilaginous fishes. TEs uniquely contribute to SVs both directly through transposition and indirectly by mediating ectopic recombination, with the proportion of TE-mediated SVs influenced by both genomic TE density and diversity. We identify >10,000 instances of recent TE turnover including extinction of LINE-2 in therian mammals and slowing of CR1 activity in passerine birds. Finally, we show that SVs have an outsized role in functional genetic variation and are >70 times more likely to strongly impact protein-coding sequences than SNVs. While SVs are on average deleterious, we identify extensive recurrent structural variation across multiple taxa in genes involved in sensory, immune, and metabolic systems. Together, this study highlights extraordinary variation in the abundance, composition, mechanism, and functional impact of SVs across vertebrates.