Essential and recurrent roles for hairpin RNAs in silencing < i > de novo < /i > sex chromosome conflict in < i > Drosophila simulans < /i >

by Jeffrey Vedanayagam, Marion Herbette, Holly Mudgett, Ching-Jung Lin, Chun-Ming Lai, Caitlin McDonough-Goldstein, Stephen Dorus, Benjamin Loppin, Colin Meiklejohn, Rapha ëlle Dubruille, Eric C. Lai Meiotic drive loci distort the normally equal segregation of alleles, which benefits their own transmission even in the face of severe fitness costs to their host organism. However, relatively little is known about the molecular identity of meiotic drivers, their strategies of action, and mechanisms that can suppress their activity. Here, we present data from the fruitflyDrosophila simulans that address these questions. We show that a family of de novo, protamine-derived X-linked selfish genes (theDox gene family) is silenced by a pair of newly emerged hairpin RNA (hpRNA) small interfering RNA (siRNA)-class loci,Nmy andTmy. In thew[XD1] genetic background, knockout ofnmy derepressesDox andMDox in testes and depletes male progeny, whereas knockout oftmy causes misexpression ofPDox genes and renders males sterile. Importantly, genetic interactions betweennmy andtmy mutant alleles reveal thatTmy also specifically maintains male progeny for normal sex ratio. We show theDox loci are functionally polymorphic withinD.simulans, such that bothnmy-associated sex ratio bias andtmy-associated sterility can be rescued by wild-type X chromosomes bearing natural deletions in differentDox family genes. Finally, using tagged transgenes ofDox andPDox2, we provide the first experimental evidence ...
Source: PLoS Biology: Archived Table of Contents - Category: Biology Authors: Source Type: research