The Drosophila melanogaster hybrid male rescue gene causes inviability in male and female species hybrids

The Drosophila melanogaster mutation Hmr rescues inviable hybrid sons from the cross of D. melanogaster females to males of its sibling species D, mau ritiana, D. simulans, and D. sechellia. We have extended previous observati ons that hybrid daughters from this cross are poorly viable at high tempera tures and have shown that this female lethality is suppressed by Hmr and th e rescue mutations In(1)AB and D. simulans Lhr. Deficiencies defined here a s Hms also suppressed lethality, demonstrating that reducing Hmr(+) activit y can rescue otherwise inviable hybrids. An Hmr(+) duplication had the oppo site effect of reducing the viability of female and sibling X-male hybrid p rogeny. Similar dose-dependent viability effects of Hmr(+) were observed in the reciprocal cross of D. simulans females to D. melanogaster males. Fina lly, Lhr and Hmr(+) were shown to have mutually antagonistic effects on hyb rid viability. These data suggest a model where the interaction of sibling species Lhr(+) and D. melanogaster Hmr+ causes lethality in both sexes of s pecies hybrids and in both directions of crossing. Our results further sugg est that a twofold difference in Hmr+ dosage accounts in part for the diffe rential viability of male and female hybrid progeny, but also that addition al, unidentified genes must be invoked to account for the invariant lethali ty of hybrid sons of D. melanogaster mothers. Implications of our findings for understanding Haldane's rule-the observation that hybrid breakdown is o ften specific to the heterogametic sex-are also discussed.