GLD-3, a Bicaudal-C homolog that inhibits FBF to control germline sex determination in C-elegans

GLD-3, a Bicaudal-C homolog that inhibits FBF to control germline sex determination in C-elegans
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DOI:
10.1016/s1534-5807(02)00322-2
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发表时间:
2002-11-01
期刊:
影响因子:
11.8
通讯作者:
Kimble, J
Kimble, J
中科院分区:
生物学1区
文献类型:
--
作者:
Eckmann, CR;Kraemer, B;Kimble, J

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FBF RNA结合蛋白控制秀丽隐杆线虫生殖系发育的多个方面,包括性别决定。FBF通过结合fem3 3'UTR中的调控元件并抑制该性别决定基因,以牺牲精子发生为代价促进卵母细胞的命运。在这里,我们报告了GLD-3的发现,GLD-3是一种与FBF物理相互作用的双头c同源细胞质蛋白。利用RNAi和gld-3缺失突变体,我们发现gld-3促进精子命运,这是一种与FBF相反的性别决定效应。上位分析表明,GLD-3作用于FBF上游,在酵母三杂交实验中,GLD-3特异性干扰FBF与fem-3 3'UTR的结合。我们建议GLD-3结合FBF,从而抑制其对目标mrna的抑制。
The FBF RNA binding proteins control multiple aspects of C. elegans germline development, including sex determination. FBF promotes the oocyte fate at the expense of spermatogenesis by binding a regulatory element in the fem-3 3'UTR and repressing this sex-determining gene. Here we report the discovery of GLD-3, a Bicaudal-C homolog and cytoplasmic protein that physically interacts with FBF. Using RNAi and a gld-3 deletion mutant, we show that GLD-3 promotes the sperm fate, a sex determination effect opposite to that of FBF. By epistasis analysis, GLD-3 acts upstream of FBF, and, in a yeast three-hybrid assay, GLD-3 interferes specifically with FBF binding to the fem-3 3'UTR. We propose that GLD-3 binds FBF and thereby inhibits its repression of target mRNAs.