Evidence of a Dual Function in Fl(2)d, a Gene Needed for Sex-Lethal Expression in Drosophila Melanogaster

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In Drosophila melanogaster, the female sexual development of the soma and the germline requires the activity of the gene Sxl. The somatic cells need the function of the gene fl(2)d to follow the female developmental pathway, due to its involvement in the female-specific splicing of Sxl RNA. Here we report the analysis of both fl(2)d(1) and fl(2)d(2) mutations: (1) fl(2)d(1) is a temperature-sensitive mutation lethal in females and semilethal in males; (2) fl(2)d(2) is lethal in both sexes; (3) the fl(2)d(1)/fl(2)d(2) constitution is temperature-sensitive and lethal in females, while semilethal in males. The temperature-sensitive period of fl(2)d(1) in females expands the whole development. Sxl(M1) partially suppresses the lethality of fl(2)d(1) homozygous females and that of fl(2)d(1)/fl(2)d(2) constitution, whereas it does not suppress the lethality of fl(2)d(2) homozygous females. The addition of extra Sxl(+) copies does not increase the suppression effect of Sxl(M1). The fl(2)d(1) mutation in homozygosis and the fl(2)d(1)/fl(2)d(2) constitution, but not the fl(2)d(2) in homozygosis, partially suppress the lethality of Sxl(M1) males. This suppression is not prevented by the addition of extra Sxl(+) copies. The semilethality of both fl(2)d(1) and fl(2)d(1)/fl(2)d(2) males, and the lethality of fl(2)d(2) males, is independent of Sxl function. There is no female synergistic lethality between mutations at fl(2)d and neither at sc or da. However, the female synergistic lethality between mutations at Sxl and either sc or da is increased by fl(2)d mutations. We have analyzed the effect of the fl(2)d mutations on the germline development of both females and males. For that purpose, we carried out the clonal analysis of fl(2)d(1) in the germline. In addition, pole cells homozygous for fl(2)d(2) were transplanted into wild-type host embryos, and we checked whether the mutant pole cells were capable of forming functional gametes. The results indicated that fl(2)d mutant germ cells cannot give rise to functional oocytes, while they can form functional sperm. Moreover, Sxl(M1) suppresses the sterility of the fl(2)d(1) homozygous females developing at the permissive temperature. Thus, with respect to the development of the germline the fl(2)d mutations mimic the behavior of loss-of-function mutations at the gene Sxl. Females double heterozygous for fl(2)d and snf(1621) are fully viable and fertile. fl(2)d(2) in heterozygosis partially suppresses the phenotype of female germ cells homozygous for snf(1621); however, this is not the case with the fl(2)d(1) mutation. The fl(2)d mutations partially suppress the phenotype of the female germ cells homozygous for ovo(D1rS1). We conclude that the gene fl(2)d has a dual function: a female-specific function involved in the splicing of Sxl RNA and a non-sex-specific function. Furthermore, the gene fl(2)d is required in the female germline for Sxl expression.

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