Monkeypox, caused by the monkeypox virus (MPXV), was historically confined to West and Central Africa but has now spread globally. Recombination and selection play crucial roles in the evolutionary adaptation of MPXV; however, the evolution of MPXV and its relationship with the recent, ground-breaking monkeypox epidemic remains poorly understood. To gain insights into the evolutionary dynamics of MPXV, comprehensive in silico recombination and selection analyses were conducted based on MPXV whole genome sequence data. Three types of recombination were identified: five ancestor-sharing interspecies recombination events, six specific interspecies recombination events and four intraspecies recombination events. The results highlight the prevalent occurrence of recombination in MPXV, with 73.3% occurring in variable regions of the genome. Selection analysis was performed from three dimensions: proteins around recombination regions, proteins from recombinant ancestors and MPXV branches, and whole-genome gene analysis. Results revealed 2 and 7 proteins under positive selection in the first two dimensions, respectively. These proteins are mainly involved in infection immunity, apoptosis regulation and viral virulence. Whole-genome analysis detected 25 genes under positive selection, mainly associated with immune response and viral regulation. Understanding their evolutionary patterns will help predict and prevent cross-species transmission, zoonotic outbreaks and potential human epidemics.

Abyssal (3501-6500 m) and hadal (>6500 m) fauna evolve under harsh abiotic stresses, characterized by high hydrostatic pressure, darkness and food shortage, providing unique opportunities to investigate mechanisms underlying environmental adaptation. Genomes of several hadal species have recently been reported. However, the genetic adaptation of deep sea species across a broad spectrum of ocean depths has yet to be thoroughly investigated, due to the challenges imposed by collecting the deep sea species. To elucidate the correlation between genetic innovation and vertical distribution, we generated a chromosome-level genome assembly of the macrourids Coryphaenoides yaquinae, which is widely distributed in the abyssal/hadal zone ranging from 3655 to 7259 m in depth. Genomic comparisons among shallow, abyssal and hadal-living species identified idiosyncratic and convergent genetic alterations underlying the extraordinary adaptations of deep-sea species including light perception, circadian regulation, hydrostatic pressure and hunger tolerance. The deep-sea fishes (Coryphaenoides Sp. and Pseudoliparis swirei) venturing into various ocean depths independently have undergone convergent amino acid substitutions in multiple proteins such as rhodopsin 1, pancreatic and duodenal homeobox 1 and melanocortin 4 receptor which are known or verified in zebrafish to be related with vision adaptation and energy expenditure. Convergent evolution events were also identified in heat shock protein 90 beta family member 1 and valosin-containing protein genes known to be related to hydrostatic pressure adaptation specifically in fishes found around the hadal range. The uncovering of the molecular convergence among the deep-sea species shed new light on the common genetic innovations required for deep-sea adaptation by the fishes.

Insect crop pests threaten global food security. This threat is amplified through the spread of nonnative species and through adaptation of native pests to control measures. Adaptations such as pesticide resistance can result from selection on variation within a population, or through gene flow from another population. We investigate these processes in an economically important noctuid crop pest, Helicoverpa zea, which has evolved resistance to a wide range of pesticides. Its sister species Helicoverpa armigera, first detected as an invasive species in Brazil in 2013, introduced the pyrethroid-resistance gene CYP337B3 to South American H. zea via adaptive introgression. To understand whether this could contribute to pesticide resistance in North America, we sequenced 237 H. zea genomes across 10 sample sites. We report H. armigera introgression into the North American H. zea population. Two individuals sampled in Texas in 2019 carry H. armigera haplotypes in a 4 Mbp region containing CYP337B3. Next, we identify signatures of selection in the panmictic population of nonadmixed H. zea, identifying a selective sweep at a second cytochrome P450 gene: CYP333B3. We estimate that its derived allele conferred a ∼5% fitness advantage and show that this estimate explains independently observed rare nonsynonymous CYP333B3 mutations approaching fixation over a ∼20-year period. We also detect putative signatures of selection at a kinesin gene associated with Bt resistance. Overall, we document two mechanisms of rapid adaptation: the introduction of fitness-enhancing alleles through interspecific introgression, and selection on intraspecific variation.

AbstractLocal adaptation frequently evolves in patches or environments that are connected via migration. In these cases, genomic regions that are linked to a locally adapted locus experience reduced effective migration rates. Via individual-based simulations of a two-patch system, we show that this reduced effective migration results in the accumulation of conditionally deleterious mutations, but not universally deleterious mutations, adjacent to adaptive loci. When there is redundancy in the genetic basis of local adaptation (i.e., genotypic redundancy), turnover of locally adapted polymorphisms allows conditionally deleterious mutation load to be purged. The amount of mutational load that accumulates adjacent to locally adapted loci is dependent on redundancy, recombination rate, migration rate, population size, strength of selection, and the phenotypic effect size of adaptive alleles. Our results highlight the need to be cautious when interpreting patterns of local adaptation at the level of phenotype or fitness, as the genetic basis of local adaptation can be transient, and evolution may confer a degree of maladaptation to nonlocal environments.

AbstractAdaptation to replicated environmental conditions can be remarkably predictable, suggesting that parallel evolution may be a common feature of adaptive radiation. An open question, however, is how phenotypic variation itself evolves during repeated adaptation. Here, we use a dataset of morphological measurements from 35 populations of threespine stickleback, consisting of 16 parapatric lake-stream pairs and three marine populations, to understand how phenotypic variation has evolved during transitions from marine to freshwater environments and during subsequent diversification across the lake-stream boundary. We find statistical support for divergent phenotypic covariance (P) across populations, with most diversification of P occurring among freshwater populations. Despite a close correspondence between within-population phenotypic variation and among-population divergence, we find that variation in P is unrelated to total variation in population means across the set of populations. For lake-stream pairs, we find that theoretical predictions for microevolutionary change can explain more than 30% of divergence in P matrices across the habitat boundary. Together, our results indicate that divergence in variance structure occurs primarily in dimensions of trait space with low phenotypic integration, correlated with disparate lake and stream environments. Our findings illustrate how conserved and divergent features of multivariate variation can underlie adaptive radiation.

Evolutionary rescue, the process by which populations facing environmental stress avoid extinction through genetic adaptation, is a critical area of study in evolutionary biology. The order in which mutations arise and get established will be relevant to the population\'s rescue. This study investigates the degree of parallel evolution at the genotypic level between independent populations facing environmental stress and subject to different demographic regimes. Under density regulation, 2 regimes exist: In the first, the population can restore positive growth rates by adjusting its population size or through adaptive mutations, whereas in the second regime, the population is doomed to extinction unless a rescue mutation occurs. Analytical approximations for the likelihood of evolutionary rescue are obtained and contrasted with simulation results. We show that the initial level of maladaptation and the demographic regime significantly affect the level of parallelism. There is an evident transition between these 2 regimes. Whereas in the first regime, parallelism decreases with the level of maladaptation, it displays the opposite behavior in the rescue/extinction regime. These findings have important implications for understanding population persistence and the degree of parallelism in evolutionary responses as they integrate demographic effects and evolutionary processes.

As modern humans ventured out of Africa and dispersed around the world, they faced novel environmental challenges that led to geographic adaptations including skin colour. Over the long history of human evolution, skin colour has changed dramatically, showing tremendous diversity across different geographical regions, for example, the majority of individuals from the expansive lands of Africa have darker skin, whereas the majority of people from Eurasia exhibit lighter skin. What adaptations did lighter skin confer upon modern humans as they migrated from Africa to Eurasia? What genetic mechanisms underlie the diversity of skin colour observed in different populations? In recent years, scientists have gradually gained a deeper understanding of the interactions between pigmentation gene and skin colour through population-based genomic studies of different groups around the world, particularly in East Asia and Africa. In this review, we summarize our current understanding of 26 skin colour-related pigmentation genes and 48 SNPs that influence skin colour. Important pigmentation genes across three major populations are described in detail: MFSD12, SLC24A5, PDPK1 and DDB1/CYB561A3/TMEM138 influence skin colour in African populations; OCA2, KITLG, SLC24A2, GNPAT and PAH are key to the evolution of skin pigmentation in East Asian populations; and SLC24A5, SLC45A2, TYR, TYRP1, ASIP, MC1R and IRF4 significantly contribute to the lightening of skin colour in European populations. We summarized recent findings in genomic studies of skin colour in populations that implicate diverse geographic environments, local adaptation among populations, gene flow and multi-gene interactions as factors influencing skin colour diversity.

Modeling the rate at which adaptive phenotypes appear in a population is a key to predicting evolutionary processes. Given random mutations, should this rate be modeled by a simple Poisson process, or is a more complex dynamics needed? Here we use analytic calculations and simulations of evolving populations on explicit genotype-phenotype maps to show that the introduction of novel phenotypes can be \"bursty\" or overdispersed. In other words, a novel phenotype either appears multiple times in quick succession or not at all for many generations. These bursts are fundamentally caused by statistical fluctuations and other structure in the map from genotypes to phenotypes. Their strength depends on population parameters, being highest for \"monomorphic\" populations with low mutation rates. They can also be enhanced by additional inhomogeneities in the mapping from genotypes to phenotypes. We mainly investigate the effect of bursts using the well-studied genotype-phenotype map for RNA secondary structure, but find similar behavior in a lattice protein model and in Richard Dawkins\'s biomorphs model of morphological development. Bursts can profoundly affect adaptive dynamics. Most notably, they imply that fitness differences play a smaller role in determining which phenotype fixes than would be the case for a Poisson process without bursts.

We know that heritable variation is abundant, and that selection causes all but the smallest populations to rapidly shift beyond their original trait distribution. So then, what limits the range of a species? There are physical constraints and also population genetic limits to the effectiveness of selection, ultimately set by population size. Global adaptation, where the same genotype is favoured over the whole range, is most efficient when based on a multitude of weakly selected alleles and is effective even when local demes are small, provided that there is some gene flow. In contrast, local adaptation is sensitive to gene flow and may require alleles with substantial effect. How can populations combine the advantages of large effective size with the ability to specialise into local niches? To what extent does reproductive isolation help resolve this tension? I address these questions using eco-evolutionary models of polygenic adaptation, contrasting discrete demes with continuousspace.

Recombination of short DNA fragments via horizontal gene transfer (HGT) can introduce beneficial alleles, create genomic disharmony through negative epistasis, and create adaptive gene combinations through positive epistasis. For non-core (accessory) genes, the negative epistatic cost is likely to be minimal because the incoming genes have not co-evolved with the recipient genome and are frequently observed as tightly linked cassettes with major effects. By contrast, interspecific recombination in the core genome is expected to be rare because disruptive allelic replacement is likely to introduce negative epistasis. Why then is homologous recombination common in the core of bacterial genomes? To understand this enigma, we take advantage of an exceptional model system, the common enteric pathogens Campylobacter jejuni and C. coli that are known for very high magnitude interspecies gene flow in the core genome. As expected, HGT does indeed disrupt co-adapted allele pairings, indirect evidence of negative epistasis. However, multiple HGT events enable recovery of the genome\'s co-adaption between introgressing alleles, even in core metabolism genes (e.g., formate dehydrogenase). These findings demonstrate that, even for complex traits, genetic coalitions can be decoupled, transferred, and independently reinstated in a new genetic background-facilitating transition between fitness peaks. In this example, the two-step recombinational process is associated with C. coli that are adapted to the agricultural niche.IMPORTANCEGenetic exchange among bacteria shapes the microbial world. From the acquisition of antimicrobial resistance genes to fundamental questions about the nature of bacterial species, this powerful evolutionary force has preoccupied scientists for decades. However, the mixing of genes between species rests on a paradox: 0n one hand, promoting adaptation by conferring novel functionality; on the other, potentially introducing disharmonious gene combinations (negative epistasis) that will be selected against. Taking an interdisciplinary approach to analyze natural populations of the enteric bacteria Campylobacter, an ideal example of long-range admixture, we demonstrate that genes can independently transfer across species boundaries and rejoin in functional networks in a recipient genome. The positive impact of two-gene interactions appears to be adaptive by expanding metabolic capacity and facilitating niche shifts through interspecific hybridization. This challenges conventional ideas and highlights the possibility of multiple-step evolution of multi-gene traits by interspecific introgression.