Sexual Dimorphism in Growth, Gene Expression, and Metabolite Profile in Early Moss Development

Sexual dimorphism evolves because selection favors different phenotypes in males and females. However, the trajectory of phenotypic evolution in species with separate sexes is determined by not just nature of selection on the two sexes, but also the correlation between the phenotypic effects of allelic substitutions in males and females. To examine these two phenomena, we studied population differentiation in males and females of the moss Ceratodon purpureus, and transcriptomic differences between males and females in early growth rate, a sexually dimorphic trait. We hypothesized that traits in which the difference between males and females evolved among populations may be subject to the strongest selection. Consistent with previous studies, we found clear evidence that the degree of sexual dimorphism evolved among populations. In contrast, we found unambiguous evidence for adaptation in male development time, but no signature of selection on the most sexually dimorphic traits. Instead, dimorphism in these traits appears to evolve because these traits exhibit sexually dimorphic correlated responses to selection on development time. These findings suggest that the genetic architecture of trait variation in males and females is quite different. To begin to understand the genetic basis of sexual dimorphism in early development, we used RNAseq to survey gene expression in ten male-female sibling pairs (i.e., two haploid plants derived from the same diploid meiosis) isolated from seven populations spanning the geographic distribution of the species. We identified a core set of ~1000 genes (both autosomal and sex-linked) that were consistently differentially expressed between females and males, of about 15,000 expressed in this tissue. These data highlight the importance of pleiotropy and genetic background in governing the phenotypic response to selection. We are currently testing these findings in other tissues to directly link sexually antagonistic selection to its molecular targets.