Granadino B, San Juán A, Santamaria P, Sánchez L
Centro de Investigaciones Biológicas, Madrid, Spain.
Genetics. 1992 Mar;130(3):597-612. doi: 10.1093/genetics/130.3.597.
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)d1 and fl(2)d2 mutations: (1) fl(2)d1 is a temperature-sensitive mutation lethal in females and semilethal in males; (2) fl(2)d2 is lethal in both sexes; (3) the fl(2)d1/fl(2)d2 constitution is temperature-sensitive and lethal in females, while semilethal in males. The temperature-sensitive period of fl(2)d1 in females expands the whole development. SxlM1 partially suppresses the lethality of fl(2)d1 homozygous females and that of fl(2)d1/fl(2)d2 constitution, whereas it does not suppress the lethality of fl(2)d2 homozygous females. The addition of extra Sxl+ copies does not increase the suppression effect of SxlM1. The fl(2)d1 mutation in homozygosis and the fl(2)d1/fl(2)d2 constitution, but not the fl(2)d2 in homozygosis, partially suppress the lethality of SxlM1 males. This suppression is not prevented by the addition of extra Sxl+ copies. The semilethality of both fl(2)d1 and fl(2)d1/fl(2)d2 males, and the lethality of fl(2)d2 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)d1 in the germline. In addition, pole cells homozygous for fl(2)d2 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, SxlM1 suppresses the sterility of the fl(2)d1 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 snf1621 are fully viable and fertile. fl(2)d2 in heterozygosis partially suppresses the phenotype of female germ cells homozygous for snf1621; however, this is not the case with the fl(2)d1 mutation. The fl(2)d mutations partially suppress the phenotype of the female germ cells homozygous for ovoDIrSI.(ABSTRACT TRUNCATED AT 400 WORDS)
在黑腹果蝇中，躯体和生殖系的雌性性发育需要Sxl基因的活性。由于fl(2)d基因参与Sxl RNA的雌性特异性剪接，体细胞需要该基因的功能才能遵循雌性发育途径。在此，我们报告了对fl(2)d1和fl(2)d2突变的分析：(1) fl(2)d1是一个温度敏感突变，对雌性致死，对雄性半致死；(2) fl(2)d2在两性中均致死；(3) fl(2)d1/fl(2)d2组合是温度敏感的，对雌性致死，对雄性半致死。雌性中fl(2)d1的温度敏感期贯穿整个发育过程。SxlM1部分抑制fl(2)d1纯合雌性以及fl(2)d1/fl(2)d2组合的致死性，而不抑制fl(2)d2纯合雌性的致死性。额外添加Sxl+拷贝不会增加SxlM1的抑制效果。纯合的fl(2)d1突变和fl(2)d1/fl(2)d2组合，但不是纯合的fl(2)d2，部分抑制SxlM1雄性的致死性。额外添加Sxl+拷贝并不能阻止这种抑制。fl(2)d1和fl(2)d1/fl(2)d2雄性的半致死性以及fl(2)d2雄性的致死性与Sxl功能无关。fl(2)d突变与sc或da突变之间不存在雌性协同致死性。然而，fl(2)d突变会增加Sxl与sc或da突变之间的雌性协同致死性。我们分析了fl(2)d突变对雌性和雄性生殖系发育的影响。为此，我们对生殖系中的fl(2)d1进行了克隆分析。此外，将fl(2)d2纯合的极细胞移植到野生型宿主胚胎中，并检查突变的极细胞是否能够形成功能性配子。结果表明，fl(2)d突变的生殖细胞不能产生功能性卵母细胞，但能形成功能性精子。此外，SxlM1抑制在允许温度下发育的fl(2)d1纯合雌性的不育性。因此，就生殖系发育而言，fl(2)d突变模拟了Sxl基因功能丧失突变的行为。fl(2)d和snf1621的双杂合雌性完全存活且可育。杂合的fl(2)d2部分抑制snf1621纯合雌性生殖细胞的表型；然而，fl(2)d1突变并非如此。fl(2)d突变部分抑制ovoDIrSI纯合雌性生殖细胞的表型。(摘要截短于400字)
