A sex-ratio Meiotic Drive System in Drosophila simulans. I: An Autosomal Suppressor

• Type of Material: Article
• Authors: Yun Tao, Emory University; John P Masly, University of Rochester; Luciana Araripe, Harvard University; Yeyan Ke, Harvard University; Daniel L Hartl, Harvard University
• Language: English
• Date: 2007-11
• Publisher: Public Library of Science
• Publication Version: Final Published Version
• Copyright Statement: © 2007 Tao et al.
• License: Creative Commons Attribution 3.0 Unported
• Final Published Version (URL): http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.0050292
• Title of Journal or Parent Work: PLoS Biology
• ISSN: 1544-9173
• Volume: 5
• Issue: 11
• Start Page: e292
• End Page: e292
• Grant/Funding Information: This work was funded by grants from the National Institutes of Health to DLH and YT (GM65169), to JPM (GM51932 through H. Allen Orr); and an Emory University Research Council grant to YT.
• Research Categories: Biology, General; Biology, Cell

Abstract

Sex ratio distortion (sex-ratio for short) has been reported in numerous species such as Drosophila, where distortion can readily be detected in experimental crosses, but the molecular mechanisms remain elusive. Here we characterize an autosomal sex-ratio suppressor from D. simulans that we designate as not much yang (nmy, polytene chromosome position 87F3). Nmy suppresses an X-linked sex-ratio distorter, contains a pair of near-perfect inverted repeats of 345 bp, and evidently originated through retrotransposition from the distorter itself. The suppression is likely mediated by sequence homology between the suppressor and distorter. The strength of sex-ratio is greatly enhanced by lower temperature. This temperature sensitivity was used to assign the sex-ratio etiology to the maturation process of the Y-bearing sperm, a hypothesis corroborated by both light microscope observations and ultrastructural studies. It has long been suggested that an X-linked sex-ratio distorter can evolve by exploiting loopholes in the meiotic machinery for its own transmission advantage, which may be offset by other changes in the genome that control the selfish distorter. Data obtained in this study help to understand this evolutionary mechanism in molecular detail and provide insight regarding its evolutionary impact on genomic architecture and speciation.