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Abstract Traits that have lost function sometimes persist through evolutionary time. Persistence may occur if there is not enough standing genetic variation for the trait to allow a response to selection, if selection against the trait is weak relative to drift, or if the trait has a residual function. To determine the evolutionary processes shaping whether nonfunctional traits are retained or lost, we investigated short stamens in 16 populations of Arabidopsis thaliana along an elevational cline in northeast Spain. A. thaliana is highly self-pollinating and prior work suggests short stamens do not contribute to self-pollination. We found a cline in short stamen number from retention of short stamens in high-elevation populations to incomplete loss in low-elevation populations. We did not find evidence that limited genetic variation constrains short stamen loss at high elevations, nor evidence for divergent selection on short stamens between high and low elevations. Finally, we identified loci associated with short stamens in northeast Spain that are different from loci associated with variation in short stamens across latitudes from a previous study. Overall, we did not identify the evolutionary mechanisms contributing to an elevational cline in short stamen number so further research is clearly warranted. 

Abstract Sexual dichromatism is thought to evolve primarily as a function of sexual selection, especially female choice. However, other forces, from sex-specific environmental conditions to social signaling in females, can also generate color differences between sexes. We studied dewlap dichromatism across 292 species of Anolis lizards. Dewlaps are colorful throat ornaments found on males of most anole species but are also present in females in many species. Although male and female dewlaps often have similar coloration, in some species, they are strikingly dichromatic. We found that ornament color is labile and that dichromatism results from the loss of costly pigments in females. This pattern could indicate a shift towards signal loss in females; however, the secondary gains of female dewlaps across the phylogeny suggest a potential advantageous function. Possible mechanisms for female dewlap coloration include social selection, nonsexual signaling, or detectability in different microhabitats (e.g., sensory drive). Female dewlap color overlap between co-occurring species is both less than expected by chance overall and reduced in species-rich communities, suggesting that dichromatism could be driven by competition. Our results highlight that selection on females drives the observed pattern of dichromatism, suggesting a potentially adaptive role for female ornaments and emphasizing the need for additional work to understand female ornament evolution. 

Abstract Sexual antagonism occurs when males and females differ in their phenotypic fitness optima but are constrained in their evolution to these optima because of their shared genome. The sex chromosomes, which have distinct evolutionary “interests” relative to the autosomes, are theorized to play an important role in sexually antagonistic conflict. However, the evolutionary responses of sex chromosomes and autosomes have usually been considered independently, that is, via contrasting the response of a gene located on either an X chromosome or an autosome. Here, we study the coevolutionary response of the X chromosome and autosomes to sexually antagonistic selection acting on a polygenic phenotype. We model a phenotype initially under stabilizing selection around a single optimum, followed by a sudden divergence of the male and female optima. We find that, in the absence of dosage compensation, the X chromosome promotes evolution toward the female optimum, inducing coevolutionary male-biased responses on the autosomes. Dosage compensation obscures the female-biased interests of the X, causing it to contribute equally to male and female phenotypic change. We further demonstrate that fluctuations in an adaptive landscape can generate prolonged intragenomic conflict and accentuate the differential responses of the X and autosomes to this conflict.