Journal of Evolutionary Biology最新文献

Genetic variation in immune genes is an important component of genetic diversity. The genes in the major histocompatibility complex (MHC) provide an excellent model system for studying the mechanisms that generate and maintain genetic diversity in natural populations. While both demographic factors and pathogen-mediated selection processes contribute to the extreme diversity observed in the MHC systems, determining the relative importance of these evolutionary mechanisms has remained challenging. We investigated the role of pathogen-mediated selection in driving MHC diversity in 3 amphibian species: Ichthyosaura alpestris, Pleurodeles waltl, and Pelophilax perezi. Our study examined the relationships between individual MHC diversity, infection status, infection intensity, and co-infection with 2 major amphibian pathogens: Batrachochytrium dendrobatidis (Bd) and Ranavirus sp. (Rv) in natural populations. Our research demonstrated significant differences in Bd and Rv infection intensities among individuals with varying numbers of MHC loci. However, co-infection showed no discernible influence on infection intensities. We observed stronger associations of specific MHC alleles and supertypes with infection intensity and status in I. alpestris. These findings suggest that, in the context of multi-host infections, MHC genes may provide valuable insights into the evolutionary forces shaping MHC diversity, although the specific effects of individual MHC alleles on disease dynamics are yet to be clarified.

Sequence variation in mitochondrial DNA (mtDNA) was once considered neutral, but growing evidence indicates it can influence metabolic, physiological, and life-history traits. Two hypotheses offer explanations for this non-neutral mtDNA variation: the mitochondrial climatic adaptation hypothesis, which posits that natural selection shapes mtDNA variation to match local environments, and the mother's curse hypothesis, which predicts the accumulation of male-harming variants due to maternal inheritance. We explored these hypotheses using genetic strains of Drosophila melanogaster bearing eight mtDNA haplotypes-nested within two distinct haplogroups (A1 and B1) that segregate along an Australian latitudinal cline. We measured the longevity of flies under cool (18°C) and warm (28°C) conditions, predicting that the A1 haplogroup-which has been reported to predominate at subtropical latitudes-would confer higher longevity in warm but reduced longevity in cool temperatures relative to the B1 counterpart. We also tested whether effects of mtDNA haplotype on longevity were larger in males, as predicted under the mother's curse hypothesis. We found mtDNA haplogroup and haplotype is associated with longevity, with the magnitude of effects varying with temperature, but not in a pattern consistent with either hypothesis. Haplogroup-by-environment interactions did not align with reported spatial distributions of the haplogroups, and haplotype effects on longevity were similar across sexes. Our findings add to the growing evidence that mtDNA variation contributes to thermal plasticity in longevity, but do not provide clear insight into whether this variation is adaptive or maladaptive.

This paper models the genetical evolution of individual behaviour rules that guide the choice of strategies in pairwise assortative interactions under incomplete information. Building on results at the cross-roads of evolutionary theory and game theory, it is first shown that in an uninvadable population state of behaviour rule evolution, individuals are compelled to use strategies that are Nash equilibria of a lineage fitness game. Thus, choice behaviour evolves to be representable as the maximization of a utility function, as if each individual holds a personal rational preference. Second, the paper contrasts two representations of personal utility that are found to be uninvadable. The first is semi-Kantian in form. This preference averages a fitness self-interest with a Kantian interest, where the average involves the genetic relatedness between interacting individuals. The Kantian interest evaluates the consequence of own behaviour for own fitness, assuming the interaction partner adopts the same behaviour as self. The second preference is a personal inclusive fitness. This preference combines a self-regarding interest with a relatedness weighted other-regarding interest. Each of these interests takes the form of an average effect, which evaluates the consequence of expressing own behaviour, instead of average population behaviour, on a statistical average fitness to self and the interaction partner, respectively.

Plasticity plays an important role in species persistence under environmental change. Morphological traits are well known to respond to various ecological factors such as temperature and predation, but less is known about the effect of social cues. In this study, we test the impact of both predator and social environmental cues on the development of male body colouration in Trinidadian guppies (Poecilia reticulata) adapted to different predation regimes. We raised second-generation (F2) fish adapted to either a high or low predation environment in a full-sibling experimental design under two crossed environments: a predator treatment (with or without predator cues) and a social treatment (isolated, or with adult tutors from their predation regime, or the opposite). Guppies adapted to a low-predation environment had a greater relative area of orange colour than high-predation guppies, repeating previous results indicating a genetic basis to male colouration. Surprisingly, predator cues had no effect on conspicuous colouration, yet social cues had a strong effect. Fish reared in isolation (regardless of population) showed more orange and black body colouration than fish reared with tutors. These results emphasize the importance of examining plasticity under complex environmental contexts and suggest a role of social dynamics in the development of trait diversity in nature. This information will contribute to our broader understanding of the interacting role of genetics and plasticity in species' responses to environmental change.

For a striking example of mitochondrial behaviour beyond adenosine triphosphate (ATP) generation, consider mitochondrion-related organelles (MROs). Hydrogenosomes, mitosomes, and other reduced mitochondrial forms have evolved through the loss of physical and functional features, from individual electron transport chain complexes to oxidative phosphorylation and the very ability to produce ATP (and further). Reduction of mitochondria is a dramatic example of convergent evolution, occuring in every eukaryotic kingdom and many parallel times. Here, we use hypercubic inference, a class of methods from evolutionary accumulation modelling, to explore the pathways of convergent mitochondrial reduction across eukaryotes. We find that most MRO diversity can be explained by small variations on two distinct pathways, starting with either the loss of Complex I or the loss of Complexes III/IV or TCA cycle steps, which tend to proceed over different characteristic timescales. We show that different clades, including ciliates and apicomplexans, reflect particular instances of these pathways. Using metabolic modelling, we connect the structure of these evolutionary pathways to the metabolic impact of the changes involved, suggesting a plausible explanation for the dramatically convergent nature of reductive evolution. We discuss this approach in connection with related theory on the genetic and functional reduction of mitochondria across organisms.

Mitochondrial RNA editing has evolved independently in numerous eukaryotic lineages, where it generally restores conserved sequences and functional reading frames in mRNA transcripts derived from altered or disrupted mitochondrial protein-coding genes. In contrast to this "restorative" RNA editing in mitochondria, most editing of nuclear mRNAs introduces novel sequence variants and diversifies the proteome. This Perspective addresses the hypothesis that these completely opposite effects of mitochondrial vs. nuclear RNA editing arise from the enormous difference in gene number between the respective genomes. Because mitochondria produce a much smaller transcriptome, they likely create less opportunity for off-target editing, which has been supported by recent experimental work expressing mitochondrial RNA editing machinery in foreign contexts. In addition, there is recent evidence that the size and complexity of RNA targets may slow the kinetics and reduce efficiency of on-target RNA editing. These findings suggest that efficient targeting and a low risk of off-target editing have facilitated the repeated emergence of disrupted mitochondrial genes and associated restorative RNA editing systems via (potentially non-adaptive) evolutionary pathways that are not feasible in larger nuclear transcriptomes due to lack of precision.

Divergent adaptation can promote ecological speciation if hybrids have reduced fitness because they are poorly adapted to either parental niche. We tested for ecologically dependent, postzygotic isolation between two subspecies of Swainson's thrushes, which form a migratory divide and hybrid zone in western North America. To do this, we translocated backcrossed and admixed birds from the hybrid zone into the range of each subspecies in the beginning of fall migration. We estimated a proxy for their survival on migration and migratory behaviour using automated radio tracking. Apparent survival of birds in the two environments did not depend on their genomic ancestry, suggesting that Swainson's thrushes' divergent adaptation to different fall migration routes does not fit the classic model of ecological speciation. We propose an alternate scenario where ecological selection on migration may interact with intrinsic maladaptation in hybrids to cause hybrid survival on migration. By translocating birds from the same genomic backgrounds into different environments, our experiment also allowed us to distinguish between the effects of environmental relative to genetic contributors to their migratory behaviour. We found evidence that both genetic and environmental factors influence migratory behaviour, as an effect of genomic ancestry on initial migratory trajectories depended on the start location for migration but birds ultimately followed expected routes given their genomic ancestries.

Sexual selection is responsible for the evolution of exaggerated morphologies in males of many animal species. In extreme cases, this has led to the emergence of novel morphs, which differ discretely from ancestral phenotypes. Morphological studies of sexually selected traits in males have mainly focused on species in which trait expression is continuous. How trait expression varies in species with discrete male morphs is comparably understudied. We find that wingless and winged male morphs in the ant Cardiocondyla obscurior differ in size and variation of eight morphological traits, including mandibles used as weapons in fights between wingless males. Differences between morphs were consistent across populations, but the size of some traits varied by population origin, even though all animals were lab-reared under identical conditions. In contrast to weapons in males of many other species, the mandibles of wingless males showed negative allometry with body size. Mandibles exhibited similar levels of fluctuating asymmetry in both morphs; in wingless males, mandible asymmetry was negatively correlated with mandible length, suggesting that stable mandible development may be an indicator of overall quality of fighter males. Mandible length showed less variation in wingless males than in winged males, whereas all other traits were more variable in wingless males, including highly conserved traits, such as antenna segment number. Wingless males also exhibited more variation in trait size than female queens and workers. Together, these data point towards stabilizing selection on weapon phenotype but overall low levels of developmental stability and canalization in an evolutionarily novel ant morph.

Phylogenetic comparative methods (PCMs) are fundamental tools for understanding trait evolution across species. While linear models are widely used for continuous traits in ecology and evolution, their application to discrete traits, particularly ordinal and nominal traits, remains limited. Researchers sometimes recategorise such traits into binary traits (0 or 1 data) to make them more manageable. However, this risks distorting the original data structure and meaning, potentially reducing the information it initially contained. This paper promotes the use of phylogenetic generalised linear mixed-effects models (PGLMMs) as a flexible framework for analysing the evolution of discrete traits. We introduce the theoretical foundations of PGLMMs and demonstrate how univariate and multivariate versions of binary PGLMMs, which might be more familiar to evolutionary biologists, can be conceptually extended to model ordinal and nominal traits. Specifically, we describe ordered and unordered multinomial PGLMMs for ordinal and nominal traits, respectively. We then explain how to interpret regression coefficients and (co)variance components, including associated statistics (e.g., phylogenetic heritability and correlation) from PGLMMs for discrete traits. Using real-world examples from avian datasets, we illustrate the practical implementation of PGLMMs to reveal evolutionary patterns in discrete traits. We also provide online tutorials to guide researchers through the application of these models using Bayesian implementations in R. By making complex models more accessible, we aim to facilitate a more precise and insightful understanding of the evolution and function of discrete traits, which have received relatively limited attention in evolutionary biology so far.

Competitive intransitivity, or non-hierarchical interactions, such as those exemplified by the rock-paper-scissors game where no single competitor wins outright, has been proposed as a key mechanism for maintaining biodiversity; however, empirical evidence supporting the importance of intransitivity remains limited. Natural populations of Saccharomyces cerevisiae often include strains harboring totivirus-satellite coinfections that encode a lethal toxic glycoprotein capable of eliminating competing yeast strains. Killer strains are sparsely distributed in natural populations, despite their assumed competitive advantage. Yeast isolates occasionally exhibit toxin resistance, but it remains untested whether they can outcompete and replace killer strains. Similarly, the persistence of toxin-susceptible yeast is not well understood - particularly whether they can invade resistant populations in the absence of killers, thereby completing an intransitive loop. In a multi-year collection of yeast isolates from vineyards across New Zealand, we observed a near-complete disappearance of a previously common killer yeast genotype of S. cerevisiae over consecutive years. Using space-time-shift competition assays, we demonstrate that strains sympatric to this killer genotype were ubiquitously resistant, unlike the allopatric strains that were frequently eliminated in competition assays. Furthermore, the extinction of the focal killer genotype appears to have enabled the emergence of toxin-susceptible competitors in sites formerly occupied by the killer genotype. Our findings suggest that the competitive advantage of toxin production is evident in natural populations but appears to be eroded when resistance evolves in competitors of the focal killer genotype. We suggest that such killer-resistant-susceptible polymorphisms are being maintained by evolutionary dynamics akin to rock-paper-scissors-like intransitivity, driven by the invasion of susceptible strains after costly resistance has driven killer strains to extinction in natural populations, all being driven by toxin-encoding coinfections.