Functional evidence that a recently evolved Drosophila sperm-specific gene boosts sperm competition
- aDepartment of Ecology and Evolutionary Biology, University of California, Irvine CA 92697;
- bDepartament de Genètica and Institut de Recerca de la Biodiversitat, Universitat de Barcelona, 08028 Barcelona, Spain;
- cDipartimento di Biologia e Biotecnologie Charles Darwin and Istituto Pasteur-Fondazione Cenci Bolognetti, Università di Roma “La Sapienza”, 00185 Rome, Italy;
- dDepartment of Organismic and Evolutionary Biology, Harvard University, Cambridge, MA 02138; and
- eDepartment of Genetics, University of Cambridge, Cambridge CB2 3EH, United Kingdom
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Contributed by Daniel L. Hartl, December 24, 2011 (sent for review December 2, 2011)

Abstract
In many species, both morphological and molecular traits related to sex and reproduction evolve faster in males than in females. Ultimately, rapid male evolution relies on the acquisition of genetic variation associated with differential reproductive success. Many newly evolved genes are associated with novel functions that might enhance male fitness. However, functional evidence of the adaptive role of recently originated genes in males is still lacking. The Sperm dynein intermediate chain multigene family, which encodes a Sperm dynein intermediate chain presumably involved in sperm motility, originated from complex genetic rearrangements in the lineage that leads to Drosophila melanogaster within the last 5.4 million years since its split from Drosophila simulans. We deleted all the members of this multigene family resident on the X chromosome of D. melanogaster by chromosome engineering and found that, although the deletion does not result in a reduction of progeny number, it impairs the competence of the sperm in the presence of sperm from wild-type males. Therefore, the Sperm dynein intermediate chain multigene family contributes to the differential reproductive success among males and illustrates precisely how quickly a new gene function can be incorporated into the genetic network of a species.
Footnotes
↵1S.-D.Y. and T.D. contributed equally to this work.
- ↵2To whom correspondence may be addressed. E-mail: dhartl{at}oeb.harvard.edu or jranz{at}uci.edu.
Author contributions: S.-D.Y., D.L.H., J. Roote, and J.M.R. designed research; S.-D.Y., T.D., C.C., A.C., F.C., E.A.Y., M.A., K.A.G., P.L., E.D., P.D., J. Rozas, and J.M.R. performed research; S.-D.Y., P.L., E.D., P.D., J. Rozas, and J.M.R. analyzed data; and S.-D.Y., D.L.H., and J.M.R. wrote the paper.
The authors declare no conflict of interest.
This article contains supporting information online at www.pnas.org/lookup/suppl/doi:10.1073/pnas.1121327109/-/DCSupplemental.