Effect of drop‐dead mutations on fertility and embryogenesis in Drosophila

Mutations in the Drosophila gene drop‐dead ( drd ) cause reduced female fertility. Females homozygous for severe alleles are sterile. In contrast, females homozygous for the mild allele drd G3 are fertile, but it is not known whether fertility is reduced. We found that 87% of eggs laid by drd G3 homozygotes hatched into larvae; this rate was not reduced relative to heterozygous controls. Therefore, drd G3 does not appear to affect fertility. In a screen for modifiers of drd , we had identified the deficiency Df(2R)Jp1 as an enhancer of adult lethality: drd G3 ;Df(2R)Jp1/+ males have significantly shorter lifespans than mutants lacking the deficiency. In the current study, we measured fertility of drd G3 /drd G3 ; Df(2R)Jp1/+ females. Only 33% of eggs laid by mutant flies with the deficiency hatched, compared with 71% of eggs laid by mutant flies without the deficiency. There may be a common biochemical pathway underlying the effects of drd on both adult survival and embryogenesis. We have previously found that eggs laid by females homozygous for the most severe alleles of drd arrest before gastrulation. We have now studied embryos laid by females homozygous for the moderate allele In(1)drd X1 . These embryos appear to develop normally through gastrulation. By midway through development, however, the embryos appear to be severely abnormal, and they do not survive to hatching. Supported by 1R15 GM080682 to EMB and an NSF REU site.