Both loss-of-function and gain-of-function mutations in snf define a role for snRNP proteins in regulating Sex-lethal pre-mRNA splicing in Drosophila development.

作者: Thomas W. Flickinger , Helen K. Salz

DOI: 10.1093/GENETICS/144.1.95

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摘要: The Drosophila snf gene encodes a protein with functional homology to the mammalian U1A and U2B" snRNP proteins. Studies, based on analysis of three viable alleles, have suggested role for in establishing female-specific splicing pattern sex determination switch gene, sex-lethal. Here, we show that non-sex-specific lethal null allele is required female determination, arguing against formal possibility alleles disrupt function unrelated snf's wild-type function. Moreover, find normal cell growth and/or survival, as expected involved cell-vital process such RNA splicing. We also only one, snfJA2, partial loss-of-function mutation. other two snf1621 snfe8H, encode antimorphic proteins are mislocalized correlate their mislocalization molecular lesions mutant phenotypes. Finally, provide genetic evidence interfere autoregulatory Sex-lethal protein. Based these studies suggest model which protein, Snf, functions block recognition regulated male-specific exon.

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