Evolution Letters最新文献

Male reproductive senescence is typically characterized by a decline in the number of sperm produced and transferred by old males, a phenomenon that may be exacerbated in polygynous species where males mate multiply. However, males also transfer seminal fluid to females, and little is known about its role in modulating male reproductive senescence. Here, we explore the contributions of sperm and seminal fluid towards male reproductive senescence in a series of sequential matings, using Drosophila melanogaster. As expected, old males produce fewer offspring than young males. However, this pattern is not driven by sperm limitation: old males have more sperm and transfer similar numbers to females, compared to young males. Instead, females storing fewer sperm of old males compared to that of young males, over a long term, drives male reproductive senescence. We are able to mitigate the age-related decline in male reproductive output by supplementing females with the seminal fluid of a young male, before she mates with an old male. Similarly, we alleviate the reduction in reproductive output across sequential matings by supplementing females with seminal fluid. Our findings highlight that seminal fluid, rather than sperm number, limits reproductive success in old or multiply mating males, highlighting its underappreciated role in reproductive aging.

Anthropogenic climate change affects wild animal populations through increasing average temperatures and more frequent extreme climatic events. Endotherms have evolved the capacity to regulate their body temperature but little is still known about how they can physiologically adapt to the pace of global warming. Adaptive responses would require that heat-tolerance mechanisms, such as the capacity to withstand high body temperatures and regulate evaporative water loss, exhibit sufficient heritable genetic variation for selection to act upon. Unfortunately, the quantitative genetics of these traits in endotherms remains poorly understood. In a recent study using infrared thermography (IRT) on semi-captive ostriches, Svensson et al., (Heritable variation in thermal profiles is associated with reproductive success in the world's largest bird. Evolution Letters, 8(2), 200-211.) sought to address this knowledge gap by measuring relative heat exchange from the head and neck and assessing the link between among-individual variation in heat dissipation and reproductive fitness. We discuss how IRT serves as a valuable tool for non-invasive data collecting, highlighting its potential for field studies of the evolutionary potential of thermal tolerance. Nevertheless, interpreting IRT data is not as straightforward as it may seem and thus must be conducted carefully. For instance, body parts from which surface temperatures are measured need to be unequivocally identified as sources of dry heat exchange in order to inform on thermoregulation-something lacking in the mentioned study. Furthermore, there is still no conclusive evidence that surface temperatures reflect core body temperatures in endotherms. Critical underlying mechanisms of the heat response, such as evaporative cooling, must also be considered. Assumptions stemming from uncertain proxies of thermoregulation can obscure our understanding of the endothermic adaptation of heat-tolerance traits to rapid global warming. These considerations emphasize that, while IRT can be a valuable tool for developing quantitative genetic approaches to estimate the evolutionary potential of heat tolerance in endotherms-particularly for species most vulnerable to warming, its application warrants careful planning.

Organism responses to environmental change require coordinated changes across correlated traits, so-called syndromes. For example, animals differ in their "pace-of-life syndrome" (POLS); suites of correlated life-history, behavioral and physiological traits. But standard "gene-centric" evolutionary theory cannot explain why POLSs exist because it assumes that the expression of phenotypic traits of animals is determined by genotype-specified reaction norms; it ignores that developmental processes can bias the direction of evolution so that phenotypes no longer match genotype-by-environment interactions. Here we apply a development-centric perspective to derive new POLS hypotheses that can resolve the conflict that current POLS predictions fail to explain which species/populations are resilient to environmental change.

Social interactions profoundly shape the dynamics and functionality of microbial populations. However, mechanisms governing the regulation of cooperative or individual traits have remained elusive. Here, we investigated the regulatory mechanisms of social behaviors by characterizing the fitness of transcriptional regulator PsdR mutants in cooperating Pseudomonas aeruginosa populations. In a canonical model described previously, PsdR was shown to solely have a nonsocial role in adaptation of these populations by controlling the intracellular uptake and processing of dipeptides. In addition to these known private traits, we found that PsdR mutants also enhanced cooperation by increasing the production of quorum sensing (QS)-regulated public goods. Although private dipeptide utilization promotes individual absolute fitness, it only partially accounts for the growth advantage of PsdR mutants. The absence of the QS master regulator LasR delayed the appearance of PsdR variants in an evolution experiment. We also demonstrated that the growth fitness of PsdR mutants is determined by a combination of the QS-mediated cooperative trait and the dipeptide metabolism-related private trait. This dual trait is co-regulated by PsdR, leading to the rapid spread of PsdR variants throughout the population. In conclusion, we identified a new social model of co-regulating cooperative and private traits in PsdR variants, uncovering the social and nonsocial roles of this transcriptional regulator in cooperating bacterial populations. Our findings advance the fundamental understanding of bacterial social interactions and provide insights into population evolution, pathogen infection control and synthetic biotechnology.

Selection often favors different trait values in males and females, leading to genetic conflicts between the sexes when traits have a shared genetic basis. Such sexual antagonism has been proposed to maintain genetic polymorphism. However, this notion is based on insights from population genetic models of single loci with fixed fitness effects. It is thus unclear how readily polymorphism emerges from sex-specific selection acting on continuous traits, where fitness effects arise from the genotype-phenotype map and the fitness landscape. Here, we model the evolution of a continuous trait that has a shared genetic basis but different optima in males and females, considering a wide variety of genetic architectures and fitness landscapes. For autosomal loci, the long-term maintenance of polymorphism requires strong conflict between males and females that generates uncharacteristic sex-specific fitness patterns. Instead, more plausible sex-specific fitness landscapes typically generate stabilizing selection leading to an evolutionarily stable state that consists of a single homozygous genotype. Except for sites tightly linked to the sex-determining region, our results indicate that genetic variation due to sexual antagonism should arise only rarely and often be transient, making these signatures challenging to detect in genomic data.

Immunocompetence evolution can involve a "resistance is futile" scenario if parasite encounter rates are so high that high investment in resistance only marginally delays infection. Here, we investigate two understudied aspects of "futility": the mode of immunocompetence and sexual selection. First, immunocompetence is usefully categorized as reducing the rate of becoming infected (resistance) or reducing the negative fitness consequences of infection once it happened (tolerance). We compare the prospects of futility for resistance, tolerance, and their joint occurrence, showing that resistance futility arises with respect to parasite encounter rates, while tolerance futility arises with respect to parasite virulence. However, if the same host trait improves pleiotropically both resistance and tolerance, futility disappears altogether and immunity investment remains profitable when increasing parasite encounter rates, virulence, or both. Second, we examine how sexual selection strength impacts these findings. If one sex (typically males) is near the faster end of a fast-slow continuum of life histories, then life history patterns reflecting futility can evolve sex-specificity. The solutions often feature sexual dimorphism in immunocompetence, but not always in the direction of strong sexual selection yielding low immunity: sexual selection can select for faster and "sicker" lives, but if sexual selection also favors traits that impact parasite encounter rates, the results are strongly dependent on whether futility (along any axis) plays a role.

[This corrects the article DOI: 10.1093/evlett/qrae056.].

Seasonal migration has fascinated scientists and natural historians for centuries. While the genetic basis of migration has been widely studied across different taxa, there is little consensus regarding which genomic regions play a role in the ability to migrate and whether they are similar across species. Here, we examine the genetic basis of intraspecific variation within and between distinct migratory phenotypes in a songbird. We focus on the Common Yellowthroat (Geothlypis trichas) as a model system because the polyphyletic origin of eastern and western clades across North America provides a strong framework for understanding the extent to which there has been parallel or convergent evolution in the genes associated with migratory behavior. First, we investigate genome-wide population genetic structure in the Common Yellowthroat in 196 individuals collected from 22 locations across breeding range. Then, to identify candidate genes involved in seasonal migration, we identify signals of putative selection in replicate comparisons between resident and migratory phenotypes within and between eastern and western clades. Overall, we find wide-spread support for parallel evolution at the genic level, particularly in genes that mediate biological timekeeping. However, we find little evidence of parallelism at the individual SNP level, supporting the idea that there are multiple genetic pathways involved in the modulation of migration.

Recent methodological approaches have expanded our understanding of Y chromosome sequence, revealed unexpected Y diversity, and sparked a growing realization of its importance in evolutionary processes. To fully understand the diversity and importance of the Y chromosome, we suggest the need to move from a holotype Y chromosome sequence, based on a single individual and meant to represent the species, to a thorough understanding of Y chromosome haplotype diversity, its phenotypic implications, and its phylogeographic distribution. Additionally, the Y chromosome may play an important role in two key rules of speciation that have otherwise been attributed to the X, namely Haldane's Rule and the Large-X Effect. Emerging genomic tools and analytical approaches are just now giving us the means to ask how important this small, often forgotten region of the genome is in evolutionary processes.

Telomere length (TL) and/or its rate of change are popular biomarkers of senescence, as telomere dynamics are linked with survival and lifespan. However, the evolutionary potential of telomere dynamics has received mixed support in natural populations. To better understand how telomere dynamics evolve, it is necessary to quantify genetic variation in TL and how such variation changes with age. Here, we analyzed 2,083 longitudinal samples from 1,225 individuals across 16 years, collected from a wild, insular house sparrow (Passer domesticus) population with complete life history and genetic relatedness data. Using a series of "animal" models, we confirmed that TL changes with age, reflecting senescence in this population. We found TL to be repeatable (14.0%, 95% CrI: 9.1%-19.9%) and heritable (12.3%, 95% CrI: 7.5%-18.2%); and detected a genotype-by-age interaction, meaning that genotypes differ in their rate of change of TL, and additive genetic variance increases at older ages. Our findings provide empirical evidence from a wild population that supports hypotheses explaining the evolution of senescence and highlight the importance of telomere dynamics as a key biomarker of body physiology for the evolution of senescence.