Erik asked me to post an update on the research I've been pursuing since joining the Chippindale lab in 2007. Since I've been in Kingston I've been conducting work on intralocus sexual conflict in
Drosophila melanogaster. For those who aren't familiar with intralocus sexual conflict, it is related to the fact that males and females often have different reproductive interests, and therefore different phenotypic optima for a variety of traits. If antagonistic selection pressures are combined with positive intersexual genetic correlations for these traits, one or both sexes may be significantly displaced from their optimum. This displacement is known as intralocus sexual conflict, and has now been demonstrated in both natural and laboratory populations from a wide variety of taxa.
The Chippindale lab has used a powerful method for investigating intralocus sexual conflict: male-limited (ML) evolution in Drosophila melanogaster. When expression of specific haploid genomes was limited to males for over 80 generations, this resulted in an increase in fitness in ML males, and a parallel decrease in fitness in ML females. The phenotypic basis for these fitness differences has been shown to be linked to a displacement of both sexes closer to the male optimum in developmental time, body size, and reproductive behaviour. In addition, it has been demonstrated that intralocus sexual conflict can actually cancel out fitness benefits of sexual selection. When high quality females were mated to high quality males (as would be expected from female choice), this resulted in the production of low-quality offspring, due to the effects of intralocus sexual conflict.
After arriving at Queen's I started an investigation of patterns of phenotypic masculinization in ML flies. I also looked for evidence of increased developmental stability in experimental populations. Using geometric morphometric analysis of wing morphology, I found evidence of masculinization of wing size and wing shape in ML flies of both sexes. I also found increased developmental stability in ML males, which seems to have resulted in decreased developmental stability in ML females. This nicely parallels the results for fitness, where ML males had increased fitness and ML females had decreased fitness (relative to controls).
Because the ML lines had been maintained for over 80 generations when I arrived in 2007 there were concerns about their continued viability, and they were terminated shortly after I started working at Queen's. Once my analysis of wing morphology was finished I therefore decided to start a new male-limited evolution experiment of my own, this time focussing on the X-chromosome. This MLX experiment will also allow me to look at imprinting effects on fitness due to the nature of the experimental evolution protocol.
The protocol for ML X-chromosome evolution is as follows:
Males are mated to females with a double X-chromosome. These DX females (DX = double X) have two X-chromosomes connected at the centromere. They also possess a Y chromosome, so when DX females are mated to normal males, they produce sons that have inherited the Y chromosome from their mothers and the X-chromosome from their fathers. Triple-X and double-Y individuals are not viable. See figure (paternal sex chromosomes are shown in blue, maternal in red, and autosomes in grey).
This father-son transmission of the X-chromosome means that individual X-chromosomes are never expressed in females as long as males are mated to DX females generation after generation. Crucially, this results in male-limited evolution of the X-chromosome. In order to avoid clonal evolution approximately 4-10% recombination between X-chromosomes is allowed using a “recombination box” protocol (see Prasad et al., 2007 for details). This experiment is simultaneously being carried out for two different source populations (LH and Ives) which have completely different histories and culturing protocols. Within each source population I have three replicate populations of selected and control flies, with effective population sizes of 480 individuals for the LH populations and approximately 1500 individuals for the Ives populations. X-chromosomes are usually transmitted from father to daughter, so the father-son transmission generated by this experimental design means that it can be extended to investigate the importance of genomic imprinting to intralocus sexual conflict.
I expect to find similar results to the previous ML experiment (i.e. an increase in male fitness and decrease in female fitness) since the X-chromosome is predicted to be particularly rich in sexually antagonistic loci. I also expect to find a decrease in male fitness due to father-transmission of the X-chromosome. Since X's are usually transmitted father to daughter, you can expect that males might imprint their X chromosomes to benefit female fitness. A male with an X primed to be in a female may therefore have reduced fitness, and some preliminary evidence collected by Stéphanie Bedhomme (a former postdoc in the Chippindale lab) is consistent with this. Perhaps the most interesting aspect of this study is that the MLX evolution protocol will potentially allow short-term evolution of the genomic imprint to adapt to father-son transmission. This is something I will also investigate. I'm currently in the middle of a preliminary fitness assay to investigate imprinting effects. I'm also planning a collaboration with Ted Morrow in Uppsala to look at differences in gene expression due to MLX evolution. I can post more about this later on.
So that's it for now. I'm also planning on running a reciprocal female-limited X-chromosome evolution experiment later on if possible, but I can write more about that later in that case.
