In WP1, we used a balancer chromosome to enforce matrilineal inheritance of the X chromosome, which eliminates male-specific selection and should result in feminization. We found evidence of phenotypic feminization in several traits, and genomic data suggested that in particular genes related to metabolism changed in expression. These changes seemed to result in a change in the genetic architecture, specifically a breakdown of the intersexual genetic correlation for locomotory activity. When females carrying one or two copies of an evolved X were compared, several phenotypic traits showed evidence of non-additivity. However, as work within WP1 progressed, it became clear that there were confounding effects of the FM balancer that was used to enforce matrilineal inheritance of the X chromosome, specifically increased female control over mating rates. Although initially disappointing, this discovery turned out to be highly interesting, since it allowed us to investigate the interactive effects of sexual antagonism and sexual conflict. By comparing the pattern of differences between the selection regimes, we were able to determine whether traits are mainly subject to sexual antagonism, sexual conflict, or a combination of the two.
In WP2 we were able to show that, surprisingly, males with mis-matched sex chromosomes had higher fitness than males with coevolved sex chromosomes. To follow up on this finding, we developed a novel mathematical model of coevolutionary cycles between the X and Y. We were able to show that coevolutionary cycles involving the X and Y chromosomes are favoured compared to coevolution between the Y and the autosomes.
In WP3 we found that there was indeed evidence of genetic variance for fitness in this species, but contrary to my initial expectation, there was no evidence of a negative genetic correlation fitness. We also carried out a follow-up experiment which found that variance in male fitness was increased under food restriction, while variance in female fitness was increased under osmotic stress.
In WP4 we carried out sex-limited selection in a hermaphrodite and found evidence of sexual specialization in gene expression, genital morphology, and behaviour, and metabolic gene expression. In addition, we found evidence of changes in recombination rate consistent with sexual specialization, which was an unexpected but highly interesting finding.
In WP5, we developed models of sexual antagonism in hermaphrodites as well as models of the establishment of inversions on sex chromosomes, and were able to show that different types of selective advantage give rise to different distributions of inversion sizes, but that they are dependent on the physical location of the sex determining locus. These models can now be combined with genomic data to test hypotheses about the evolution of recombination cessation.
The project has resulted in the production of 4 PhD theses, 8 papers, 2 preprints, and 2 other submitted manuscripts to date. A number of additional manuscripts are in preparation. Information about the results from the project has also been disseminated via national and international conferences. Finally, information has been disseminated to the public via several popular science lectures.
