Control of meiotic cell cycle progression in males

控制雄性减数分裂细胞周期进程

• 批准号: 6887018
• 负责人: Catherine Craig Baker
• 金额: $ 4.4万
• 依托单位: STANFORD UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2005
• 资助国家: 美国
• 起止时间: 2005-09-15 至 2007-09-14
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6887018
• 关键词: Drosophilidae; RNA binding protein; antibody; arthropod genetics; cell cycle proteins; cell growth regulation; chemical stability; chimeric proteins; developmental genetics; gene deletion mutation; gene induction /repression; genetic regulation; genetic translation; immunoprecipitation; in situ hybridization; laboratory rabbit; male; meiosis; microarray technology; phosphoprotein phosphatase; point mutation; postdoctoral investigator; protein localization; protein sequence; transcription factor; yeast two hybrid system

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.

描述(由申请人提供)： 我在这里提出的研究将解决发育信号如何调节细胞周期的一般问题，具体目标是研究使雄性果蝇减数分裂延迟直到所有精子细胞分化基因转录完成的途径(S)。几个实验室的初步工作表明，雄性减数分裂特异的CDC25 Twin在G2/M转换中发挥了重要作用。已知减数分裂的开始需要Twin的活性；此外，TWINE的翻译依赖于几个基因的野生型功能，包括三个编码睾丸特异的TBP相关因子(TAFs、Can、Mia和Sa)和一个RNA结合蛋白(Boule)。这里提出的工作将解决转录因子、Boule和TWINE翻译之间的联系。首先，我将确定Boule蛋白积累受到控制的机制，因为已知在sa和mia突变体中不存在Boule蛋白积累。其次，我将对游击手突变体进行表征，并研究其野生型产物的分子作用模式。