Carleton Biology Talks: Dr. Adam Chippindale

Carleton Biology Talks: Dr. Adam Chippindale

Categories: Lectures and Seminars | Intended for

Friday, November 07, 2014

3:30 PM - 4:30 PM | Add to calendar

4440Q Carleton Technology and Training Centre

1125 Colonel By Dr, Ottawa, ON

Contact Information

Andrew Simons, 613-520-2600, andrew.simons@carleton.ca

Registration

No registration required.

Cost

Free

About this Event

Host Organization: Biology Department
More Information: Please click here for additional details.

Mother's curse and the enemies Within: Experimental evolution of sexual conflict within and between genomes.ity
Adam Chippindale, Associate Professor, Department of Biology, Queen’s University

Sexual conflict arises when the evolutionary interests of the two sexes are not aligned. This may be because the optimal timing or frequency of mating differ for females and males, or because the optimal allele (or level of gene expression) at a given locus differs. The first kind of conflict has been likened to an arms race, whereas the second kind is more like a tug-of-war between the sexes. I will summarize some recent highlights from my lab's work on sexual conflict using experimental evolution in the fruit fly Drosophila. In one series of experiments, we have eliminated selection on female Darwinian fitness, allowing males to "win" the tug-of-war. Under this Male Limited (ML) evolution treatment, male fitness increased rapidly via masculinization of a variety of measured traits; importantly, the fitness of ML-evolved chromosomes was reduced when expressed in females, and these females expressed more male-like characters. Follow up experiments revealed a strong role for the X-chromosome in the response to selection as well as an intriguing parent of origin effect which may represent the first evidence for genomic imprinting in an insect. Sexual conflict may also occur over organelles, as maternal transmission of cytoplasm via the egg creates conditions where endosymbionts should favour females, potentially at the expense of males. We tested this using 10 long-term lab evolved populations with very different optimal life histories and potentially very different demands upon the mitochiondria. We created nuclear-cytoplasmic "cybrids" by introgressing the nuclei from one type of line into the other type of cytoplasm. Our results supported the Mother's Curse hypothesis: non-coevolved mitochondria were detrimental to males only, suggesting that nuclear genes in each parent population compensate for male-specific mutations in the mitchondrion. I will discuss this result in terms of its implications for male infertility and the evolutionary simplification of endosymbionts.