Schwartzmassey5280

Evidence is mounting that climate-driven shifts in environmental conditions can elicit organismal evolution, yet there are sparingly few long-term records that document the tempo and progression of responses, particularly for plants capable of transforming ecosystems. In this study, we "resurrected" cohorts of a foundational coastal marsh sedge (Schoenoplectus americanus) from a time-stratified seed bank to reconstruct a century-long record of heritable variation in response to salinity exposure. Common-garden experiments revealed that S. americanus exhibits heritable variation in phenotypic traits and biomass-based measures of salinity tolerance. We found that responses to salinity exposure differed among the revived cohorts, with plants from the early 20th century exhibiting greater salinity tolerance than those from the mid to late 20th century. Fluctuations in salinity tolerance could reflect stochastic variation but a congruent record of genotypic variation points to the alternative possibility that the loss and gain in functionality are driven by selection, with comparisons to historical rainfall and paleosalinity records suggesting that selective pressures vary according to shifting estuarine conditions. Because salinity tolerance in S. americanus is tightly coupled to primary productivity and other vital ecosystem attributes, these findings indicate that organismal evolution merits further consideration as a factor shaping coastal marsh responses to climate change.When natural populations split and migrate to different environments, they may experience different selection pressures that can lead to local adaptation. To capture the genomic patterns of a local selective sweep, we develop XP-nSL, a genomic scan for local adaptation that compares haplotype patterns between two populations. We show that XP-nSL has power to detect ongoing and recently completed hard and soft sweeps, and we then apply this statistic to search for evidence of adaptation to high altitude in rhesus macaques. We analyze the whole genomes of 23 wild rhesus macaques captured at high altitude (mean altitude > 4000 m above sea level) to 22 wild rhesus macaques captured at low altitude (mean altitude less then 500 m above sea level) and find evidence of local adaptation in the high-altitude population at or near 303 known genes and several unannotated regions. We find the strongest signal for adaptation at EGLN1, a classic target for convergent evolution in several species living in low oxygen environments. Furthermore, many of the 303 genes are involved in processes related to hypoxia, regulation of ROS, DNA damage repair, synaptic signaling, and metabolism. These results suggest that, beyond adapting via a beneficial mutation in one single gene, adaptation to high altitude in rhesus macaques is polygenic and spread across numerous important biological systems.Quantitative genetic theory proposes that phenotypic evolution is shaped by G, the matrix of genetic variances and covariances among traits. In species with separate sexes, the evolution of sexual dimorphism is also shaped by B, the matrix of between-sex genetic variances and covariances. Despite considerable focus on estimating these matrices, their underlying biological mechanisms are largely speculative. We experimentally tested the hypothesis that G and B are structured by hormonal pleiotropy, which occurs when one hormone influences multiple phenotypes. Using juvenile brown anole lizards (Anolis sagrei) bred in a paternal half-sibling design, we elevated the steroid hormone testosterone with slow-release implants while administering empty implants to siblings as a control. We quantified the effects of this manipulation on the genetic architecture of a suite of sexually dimorphic traits, including body size (males are larger than females) and the area, hue, saturation, and brightness of the dewlap (a coloimportant yet overlooked role in mediating evolutionary responses to selection.The neural crest hypothesis posits that selection for tameness resulted in mild alterations to neural crest cells during embryonic development, which directly or indirectly caused the appearance of traits associated with the "domestication syndrome" (DS). JNJ-42226314 concentration Although representing an appealing unitary explanation for the generation of domestic phenotypes, support for this hypothesis from morphological data and for the validity of the DS remains a topic of debate. This study used the frameworks of morphological integration and modularity to assess patterns that concern the embryonic origin of the skull and issues around the neural crest hypothesis. Geometric morphometric landmarks were used to quantify cranial trait interactions between six pairs of wild and domestic mammals, comprising representatives that express between five and 17 of the traits included in the DS, and examples from each of the pathways by which animals entered into relationships with humans. We predicted the presence of neural crest vs mesodermework that promotes flexibility under the selection regimes of domestication.Hamilton's local mate competition theory provided an explanation for extraordinary female-biased sex ratios in a range of organisms. When mating takes place locally, in structured populations, a female-biased sex ratio is favored to reduce competition between related males, and to provide more mates for males. However, there are a number of wasp species in which the sex ratios appear to more female biased than predicted by Hamilton's theory. It has been hypothesized that the additional female bias in these wasp species results from cooperative interactions between females. We investigated theoretically the extent to which cooperation between related females can interact with local mate competition to favor even more female-biased sex ratios. We found that (i) cooperation between females can lead to sex ratios that are more female biased than predicted by local competition theory alone, and (ii) sex ratios can be more female biased when the cooperation occurs from offspring to mothers before dispersal, rather than cooperation between siblings after dispersal. Our models formally confirm the verbal predictions made in previous experimental studies, which could be applied to a range of organisms. Specifically, cooperation can help explain sex ratio biases in Sclerodermus and Melittobia wasps, although quantitative comparisons between predictions and data suggest that some additional factors may be operating.The majority of the genome is shared between the sexes, and it is expected that the genetic architecture of most traits is shared as well. This common architecture has been viewed as a major source of constraint on the evolution of sexual dimorphism (SD). SD is nonetheless common in nature, leading to assumptions that it results from differential regulation of shared genetic architecture. Here, we study the effect of thousands of gene knockout mutations on 202 mouse phenotypes to explore how regulatory variation affects SD. We show that many traits are dimorphic to some extent, and that a surprising proportion of knockouts have sex-specific phenotypic effects. Many traits, regardless whether they are monomorphic or dimorphic, harbor cryptic differences in genetic architecture between the sexes, resulting in sexually discordant phenotypic effects from sexually concordant regulatory changes. This provides an alternative route to dimorphism through sex-specific genetic architecture, rather than differential regulation of shared architecture.Despite the far-reaching evolutionary implications of sexual conflict, the effects of metapopulation structure, when populations are subdivided into several demes connected to some degree by migration, on sexual conflict dynamics are unknown. Here, we used experimental evolution in an insect model system, the seed beetle Callosobruchus maculatus, to assess the independent and interacting effects of selection histories associated with mating system (monogamy vs. polygamy) and population subdivision on sexual conflict evolution. We confirm traditional predictions from sexual conflict theory by revealing increased resistance to male harm in females from populations with a history of intense sexual selection (polygamous populations) compared to females from populations with a history of relaxed sexual selection (monogamous populations). However, selection arising from metapopulation structure reversed the classic pattern of sexually antagonistic coevolution and led to reduced resistance in females from polygamous populations. These results underscore that population spatial structure moderates sexual selection and sexual conflict, and more broadly, that the evolution of sexual conflict is contingent on ecological context. The findings also have implications for population dynamics, conservation biology, and biological control.Theory predicts that the ability of selection and recombination to purge mutation load is enhanced if selection against deleterious genetic variants operates more strongly in males than females. However, direct empirical support for this tenet is limited, in part because traditional quantitative genetic approaches allow dominance and intermediate-frequency polymorphisms to obscure the effects of the many rare and partially recessive deleterious alleles that make up the main part of a population's mutation load. Here, we exposed the partially recessive genetic load of a population of Callosobruchus maculatus seed beetles via successive generations of inbreeding, and quantified its effects by measuring heterosis-the increase in fitness experienced when masking the effects of deleterious alleles by heterozygosity-in a fully factorial sex-specific diallel cross among 16 inbred strains. Competitive lifetime reproductive success (i.e., fitness) was measured in male and female outcrossed F1s as well as inbred parental "selfs," and we estimated the 4 × 4 male-female inbred-outbred genetic covariance matrix for fitness using Bayesian Markov chain Monte Carlo simulations of a custom-made general linear mixed effects model. We found that heterosis estimated independently in males and females was highly genetically correlated among strains, and that heterosis was strongly negatively genetically correlated to outbred male, but not female, fitness. This suggests that genetic variation for fitness in males, but not in females, reflects the amount of (partially) recessive deleterious alleles segregating at mutation-selection balance in this population. The population's mutation load therefore has greater potential to be purged via selection in males. These findings contribute to our understanding of the prevalence of sexual reproduction in nature and the maintenance of genetic variation in fitness-related traits.Although it is widely stated that both mating behavior and sperm traits are energetically costly for males, we currently lack empirical estimates of the relative costs to males of pre- versus postcopulatory investments. Such estimates require the experimental separation of the act of mating from that of ejaculation, which is a nontrivial logistical challenge. Here, we overcome this challenge using a novel morphological manipulation (gonopodium tip ablation) in the eastern mosquitofish (Gambusia holbrooki) to tease apart investment in mating effort from that in sperm replenishment following ejaculation. We quantified the relative cumulative costs of investing in mating effort and ejaculation by comparing somatic traits and reproductive performance among three types of males ablated males that could attempt to mate but not ejaculate; unablated males that could both mate and ejaculate; and control males that had no access to females. We show that, after eight weeks, mating investment significantly reduces both body growth and immunocompetence and results in a significant decline in mating effort.