307C Poster - 03. Evolution
Saturday April 09, 1:30 PM - 3:30 PM

Authors:
Sarah A. Tomlin ^1,2; Vada Becker ⁴; David M. Brinkley ³; Ching-Ho Chang ^1,2; Harmit S. Malik ^1,2

Affiliations:
1) Howard Hughes Medical Institute, HHMI, Chevy Chase, MD; 2) Fred Hutchinson Cancer Research Center, Basic Sciences, Seattle, WA; 3) University of Washington, Molecular and Cellular Biology, MCB, Seattle WA; 4) University of Washington, Molecular Medicine and Mechanisms of Disease, M3D Seattle, WA

Keywords:
d. evolution of gene expression; n. other (Mitonuclear conflict)

Mitochondria are specialized double-membrane organelles of bacterial origin present in most eukaryotic cells. Mitochondria contain circular DNA (mtDNA) almost exclusively uniparentally (maternal) inherited through females in most plants and animals. Such uniparental inheritance has been hypothesized to result in the accumulation of 'male-harming' mutations that are neutral or beneficial to females due to lack of selection (the "Mother's Curse" hypothesis). Previously, we found one such exclusively male-harming mtDNA (G177S) mutation in the cytochrome oxidase II gene (COII) of Drosophila melanogaster. G177S led to significant impairment of male fertility at 25 and 29 degrees but no impairment in female function. Over five years, the G177S mtDNA mutation was passaged without selection in the w1118 nuclear background. We found that male fertility had recovered substantially but not to wildtype levels in this line, suggesting the possibility that a de novo nuclear suppressor of male infertility arose and swept to fixation in the laboratory. Intriguingly, restoration of male fertility appeared together with lower female fertility in flies carrying the G11S mtDNA mutation. To recreate the original male infertility phenotype, we take advantage of genetic backcrosses to a w1118 line not subject to selection because it carries wildtype mtDNA instead of G1777S mtDNA. We aim to identify the genetic basis of this de novo suppression by whole genome sequencing.