Genetics, Vol. 166, 789-796, February 2004, Copyright © 2004
Genetic Complexity Underlying Hybrid Male Sterility in Drosophila
Kyoichi Sawamuraa,
John Rooteb,
Chung-I Wuc, and
Masa-Toshi Yamamotoa
a Drosophila Genetic Resource Center, Kyoto Institute of Technology, Kyoto 616-8354, Japan,
b Department of Genetics, University of Cambridge, Cambridge CB2 3EH, United Kingdom
c Department of Ecology and Evolution, University of Chicago, Chicago, Illinois 60637
Corresponding author:
Kyoichi Sawamura, University of Tsukuba, 1-1-1 Tennodai, Tsukuba 305-8572, Japan., sawamura{at}biol.tsukuba.ac.jp (E-mail)
Communicating editor: M. AGUADÉ
Recent genetic analyses of closely related species of Drosophila have indicated that hybrid male sterility is the consequence of highly complex synergistic effects among multiple genes, both conspecific and heterospecific. On the contrary, much evidence suggests the presence of major genes causing hybrid female sterility and inviability in the less-related species, D. melanogaster and D. simulans. Does this contrast reflect the genetic distance between species? Or, generally, is the genetic basis of hybrid male sterility more complex than that of hybrid female sterility and inviability? To clarify this point, the D. simulans introgression of the cytological region 34D–36A to the D. melanogaster genome, which causes recessive male sterility, was dissected by recombination, deficiency, and complementation mapping. The 450-kb region between two genes, Suppressor of Hairless and snail, exhibited a strong effect on the sterility. Males are (semi-)sterile if this region of the introgression is made homozygous or hemizygous. But no genes in the region singly cause the sterility; this region has at least two genes, which in combination result in male sterility. Further, the males are less fertile when heterozygous with a larger introgression, which suggests that dominant modifiers enhance the effects of recessive genes of male sterility. Such an epistatic view, even in the less-related species, suggests that the genetic complexity is special to hybrid male sterility.
