Molecular Ecology最新文献

Cichlids are a textbook model system of adaptive radiation and a fascinating example of rapid sex chromosome evolution. Yet in these fish, as in most other taxa, the mechanisms causing sex chromosome turnover and the subsequent impact thereof are unknown. Sexual antagonism was long thought to be a driver of sex chromosome emergence, but experimental support remains scarce. Here, we show that sex-biased genes, often used as indicators of sexual antagonism, are enriched in three different sex chromosome systems of Lake Tanganyika cichlid species that diverged less than 4 million years ago. Moreover, gene expression is feminised in species that transitioned from an XY to a ZW system on the same chromosome. This is achieved by gain of female-biased genes, increase of female sex-bias as well as decrease of male-bias depending on the tissue investigated. We further show that XY sex chromosomes have more male-biased genes but without higher intensity of sex-biased expression. A large fraction of sex-bias in gene expression evolved adaptively, with a stronger signature in females than males. While we find that sex-bias in gene expression clearly depends on the heterogametic system, we find only weak support for sex-biased expression priming chromosomes to become sex chromosomes. Overall, we conclude that there is little evidence that sexual antagonism drives sex chromosome emergence but that it likely plays a role during sex chromosome differentiation. We see rapid emergence of antagonistic expression in sex-linked genes.

In plant–virus–vector tripartite relationships, it has been recognised that viral infections alter the physiological state of host plants, enhancing vector performance and facilitating virus transmission to other host individuals. Natural tripartite systems with perennial host plants are expected to persist for a long time through clonal propagation and the spread of virus-infected hosts. Under such circumstances, viral infection may negatively affect the vector, enhancing host vigour. We used the Arabidopsis halleri–turnip mosaic virus (TuMV)-aphid system to test this hypothesis. We compared aphid performance between TuMV-infected and uninfected plants, and host transcriptomes of intact, aphid-infested, TuMV-infected, and aphid-infested TuMV-infected plants. Fewer aphids were observed on TuMV-infected plants than on uninfected plants in the natural population. Manipulative experiments revealed that aphid fecundity, but not preference or emigration, was reduced on TuMV-infected plants. The host transcriptome responses to aphids were markedly weakened in TuMV-infected plants. This attenuation occurred in the form of counter-attenuation, in which the host genes respond in opposite directions to the viruses and aphids. For example, three known host genes that promote aphid fecundity are upregulated by aphid infestation in the absence of TuMV, whereas these responses are attenuated by TuMV infection. Additionally, four genes were identified as candidate genes that may have caused the TuMV-triggered reduction in aphid fecundity. In conclusion, we showed that viral infections simultaneously suppressed aphid fecundity and host plant responses induced by aphids. These interactions may prevent the host population from collapsing and enhance the coexistence of plant–virus–vector in natural environments.

Parasites are expected to hybridise in similar ways to free-living organisms, although this may be modified by their reduced genome architecture. Recombinant strains and taxa of hybrid origin can be studied in nature where hosts come into secondary contact. Here we apply genome-wide analysis to parasites from a contact previously characterised for many individuals using classical markers. The host contact is the European house mouse hybrid zone; the parasites are lung fungus Pneumocystis and gut pinworm Syphacia. The genomic (many loci) and classical (many-individual) results are broadly consistent in scale and centring of transitions across the host hybrid zone. Whole mitogenome comparisons confirm earlier suggestions that parasite divergence is low compared to their hosts, perhaps due to reduced-genome stabilising selection. In the recombining genome, we are able to show blocks of the parasite genome of alternating host origin, including one Pneumocystis strain which appears to be an F3+ cross and one recombinant Syphacia strain found over multiple localities. Functional analyses of introgressing genes show enrichment for genes likely important for parasitic lifestyle. Our work confirms that evolutionary models of hybridisation apply equally to hosts and their parasites.

Host density, genetic diversity and social groups are key factors influencing pathogen transmission in wildlife populations, but their interactions remain poorly understood in insects. Islands can provide natural laboratories with distinct populations that vary in density and genetic diversity, whereby dense, genetically homogeneous populations are expected to facilitate pathogen transmission. We used bumble bees to test these predictions, assessing the population structure of the two common species Bombus pascuorum and B. terrestris across island and mainland sites in the British Isles and France and testing bees for five micro-parasitic and four viral pathogens. B. pascuorum formed distinct genetic clusters on islands, with varying levels of heterozygosity and only the Isle of Arran clustered with mainland populations. B. terrestris populations were less structured, but populations on the Isle of Man and the Scilly Isles were genetically separated from other island and mainland populations while showing low heterozygosity. Colony density was similar between species and not linked to genetic diversity but had a positive effect on the prevalence of some pathogens. Contrary to expectations, there was no protective effect of high genetic diversity, suggesting that generalist bumble bee pathogens could be more affected by host species diversity and density. Yet, within B. terrestris populations, we found that nestmates showed more similar pathogen profiles than unrelated individuals, suggesting that genetic similarity and high contact rates within nests affect pathogen prevalence in wild bees.

Hybridization is a widespread evolutionary process and a key source of evolutionary novelty. Despite intensive study, the extent to which hybridization is deterministic and repeatable, particularly in recurrent contact events involving the same species under varying ecological conditions, remains unclear. Here, we investigated three replicated contact zones between Scots pine (Pinus sylvestris) and dwarf mountain pine (Pinus mugo) in Central Europe: two occurring in peatland habitats and one in a contrasting sandstone outcrop. Using genome-wide SNP genotyping of over 1300 individuals, we analysed genomic structure, diversity, and ancestry patterns across these zones. All sites revealed pervasive hybridization, dominated by later-generation hybrids and a notable scarcity of pure P. mugo. Across environments, hybrid populations exhibited strikingly consistent genomic compositions, with asymmetric introgression strongly biased toward P. mugo ancestry, suggesting that hybrid genome structure may follow predictable patterns under similar ecological conditions and could be shaped by cytonuclear incompatibilities. Nonetheless, we also detected site-specific differences in hybrid diversity and phenotype, highlighting the influence of local environmental selection on shared hybrid genomic backgrounds. We provide genomic evidence that Pinus uliginosa, a morphologically distinct peat bog pine traditionally regarded as a relict and endangered species is instead a partially stabilised hybrid lineage. Its genome reflects incomplete hybridization and ecological filtering, yet it lacks sufficient genetic divergence to be recognised as a distinct species. Together, these results provide evidence for the repeatability of hybridization processes, which result in the formation of phenotypes reflecting a species continuum subjected to strong environmental pressures. The findings support the simplification of taxonomic nomenclature within the Pinus mugo complex, informing adaptive conservation strategies and the genetic management of hybrid lineages.

Resource heterogeneity is a widespread phenomenon, as resources are rarely spaced evenly across a landscape. Variation in resource density and distribution can have a myriad of behavioural, ecological, and evolutionary consequences for populations, yet clarifying these effects is still challenging. We combine both novel and previously published data on genetic parentage, relatedness, life history, and predation to present a comprehensive field study of a shell bed in Lake Tanganyika. Here, a wild population of the cichlid fish Neolamprologus multifasciatus is naturally subdivided into habitat regions that differ immensely in shelter density and distribution, as well as in the capacity for the fish to physically rearrange their shelters into clusters (i.e., engage in niche construction). Shelters were evenly, densely, and continuously spaced in one habitat, while they were highly clustered in the other habitat. We expected the environmental potential for polygyny to be greater in the clustered habitat relative to the continuous habitat. Predation regimes and life history traits differed, with N. multifasciatus in the evenly distributed habitat experiencing higher predation threats, earlier maturation, and slower growth than those in the clustered habitat. Metrics of selection, however, were surprisingly consistent between the two habitats, as were patterns of dispersal. Overall, our research leverages the natural subdivision of a wild population into distinct habitats to investigate the ecological and evolutionary implications of resource heterogeneity and habitat modification.

Recent research in humans and both model and non-model animals has shown that DNA methylation (DNAm), an epigenetic modification, is one of the mechanisms underlying the ageing process. DNAm-based indices predict mortality and provide valuable insights into biological ageing mechanisms. Although sex-dependent differences in lifespan are ubiquitous and sex chromosomes are thought to play an important role in sex-specific ageing, they have been largely ignored in epigenetic ageing studies. We characterised the genome-wide distribution of age-related CpG (Cytosine-phosphate-Guanine) sites from longitudinal samples in two avian species (zebra finch and jackdaw), including for the first time the avian sex chromosomes (Z and the female-specific, haploid W). In both species, we find a small fraction of the CpG sites to show age-related changes in DNAm with the majority of them being located on the haploid, female-specific W chromosome, where DNAm levels predominantly decrease with age. Age-related CpG sites were over-represented on the zebra finch but under-represented on the jackdaw Z chromosome. Our results highlight distinct age-related changes in sex chromosome DNAm compared to the rest of the genome in two avian species, suggesting this previously understudied feature of sex chromosomes may be instrumental in sex-dependent ageing. Moreover, studying the DNAm of sex chromosomes might be particularly useful in ageing research, facilitating the identification of shared (sex-dependent) age-related pathways and processes between phylogenetically diverse organisms.

During infection, hosts may shift resources away from reproduction towards immune defence. It is unclear to what degree these costly trade-offs can be alleviated during protective coinfections, whereby antagonism between parasites reduces disease severity. We used transcriptomics to assess the extent to which host gene expression reflected the effect of protection and whether reducing or increasing investment in immunity carried costs to reproduction. Virulent infections by Leucobacter musarum bacteria elicited greater trade-offs in nematode hosts compared to the naturally coinfecting ‘protective parasite’ Leucobacter celer. We further found that coinfection attenuated host investment in pro-immune trade-offs, without significantly changing which host genes were involved. We then sought to understand if this attenuated host response would be consistent with possible mechanisms of inter-parasite competition. Our chromosome length genome assemblies for both parasite species revealed that protective coinfection may operate by competition for public goods, such as siderophore-mediated uptake of metal ions (e.g., iron) or colonisation of the host cuticle. Ultimately, we show that competition between coinfecting parasites can complement endogenous host defences and ease the reproductive costs of fighting harmful infection.