The Drosophila snf gene is a positive regulator of the sex determination gene Sex-lethal in both the germline and the soma. Its role in the soma is only evident when the probability of Sex-lethal activation has been reduced. For instance, in an otherwise wild-type background, females homozygous for a weak snf mutation produce both male and female progeny; however, when mated to males hemizygous for a null allele of Sex-lethal, they produce only male progeny. We demonstrate that the lack of female progeny is due to aberrant Sex-lethal regulation in late embryogenesis. In these mutant embryos, there is little accumulation of the late female-specific spliced RNAs and proteins. In contrast, in early embryogenesis, Sex-lethal regulation is not affected. The accumulation of both the early Sex-lethal transcripts and proteins is normal. These results suggest that the wild-type product of snf plays an important role in establishing the female-specific RNA splicing pattern of Sex-lethal. Whether snf influences the female-specific splice site choice directly or indirectly remains to be determined.