Control of meiotic cell cycle progression in males

描述（由申请人提供）： 我在这里提出的研究将解决细胞周期如何被发育信号调节的一般问题，具体目标是研究使果蝇雄性减数分裂延迟直到所有精子细胞分化基因被转录的途径。几个实验室的初步工作表明，Twine，雄性减数分裂特异性Cdc 25，是G2/M过渡的重要参与者。已知减数分裂的开始需要Twine活性;此外，翻译TBP依赖于几个基因的野生型功能，包括三个编码睾丸特异性TBP相关因子（TAF，can，mia和sa）和RNA结合蛋白（Boule）。这里提出的工作将解决转录因子，Boule和翻译之间的联系。首先，我将确定Boule蛋白积累的控制机制，因为已知它在sa和mia突变体中不存在。其次，我将描述游击手突变体，并研究其野生型产品的分子作用模式。

DESCRIPTION (provided by applicant): The research which I propose here will address the general question of how the cell cycle can be regulated by developmental signals, with the specific goal of investigating the pathway(s) that enable the delay of meiotic division in Drosophila males until all spermatid differentiation genes are transcribed. Initial work in several labs has implicated Twine, the male meiosis-specific Cdc25, as an important player in the G2/M transition. The onset of meiotic division is known to require Twine activity; in addition, the translation of twine depends on wild-type function of several genes, including three encoding testis-specific TBP-associated factors (TAFs, can, mia, and sa), and an RNA-binding protein (Boule). The work proposed here will address the connection between the transcription factors, Boule, and twine translation. First, I will identify the mechanism by which Boule protein accumulation is controlled, since it is known to be absent in sa and mia mutants. Second, I will characterize the shortstop mutant and investigate the molecular mode of action of its wild-type product.