Sex Chromosome Evolution in a Hermaphrodite : Genetic and phenotypic relationships between sex roles

Sammanfattning: Sex chromosome evolution in a hermaphrodite ancestor starts with the establishment of a sex-determining region (SDR). Over time, sex-specific genes, and/or sexually antagonistic alleles will become linked to the SDR. Sexually antagonistic alleles are a type of genetic variation that increases fitness for one sex while being detrimental for the other sex. Recombination arrest around the SDR and genes linked to it will evolve, effectively preventing breaking up of advantageous gene combinations. Eventually, the region of recombination arrest will increase as more sex-specific genes migrate to the proto-sex chromosome, and this will in the end lead to degenerated sex chromosomes where deleterious mutations accumulate and genes are lost. However, most research to date has focused on old, already degenerated sex chromosomes, and relatively few have looked at the very initial phases of sex chromosome evolution. In this thesis, I aimed at producing a deeper understanding of the very beginning of sex chromosome evolution in a hermaphrodite ancestor. I do this both with sex-limited experimental evolution, simulating the evolution of a sex chromosome in a hermaphrodite (the simultaneous hermaphroditic flatworm Macrostomum lignano), and by examining the relationships between male and female fitness components in the study species. When mimicking the evolution of a sex chromosome, a genetic marker (GFP, green fluorescent protein) acted as a sex-determining gene. In the male-limited selection, the marker was passed through sperm (fitness through male sex role), and in the female-limited selection, it passed through eggs (i.e. fitness though female sex role). There were 4 replicate populations per treatment (male-limited, female-limited and control treatment). Here, I show that additive genetic variance for female fitness is three times larger than male fitness in stock populations of M. lignano. I also found that additive genetic variance was environment-specific, and the difference depended on the sex-role. The relationship between male and female fitness was weak both on the genetic and phenotypic level, and it did not seem to change across environments. This indicates that male and female fitness function can evolve independently from each other, and that there was no sexual antagonism between sex roles. Despite this, we could show evidence of a genetically-based trade-off in the sex-limited experimental evolution, indicating that we might have reinforced a negative intersexual genetic correlation between sex roles during the course of the experiment. Gene expression analysis also revealed that the largest number of differentially expressed genes was between the male- and female-limited selection treatments, but there was no expression difference between treatments in the sex-specific organs (antrum and prostate gland). In any case, we could show proof of concept that the early stages of sex chromosome evolution are observable in real time.