精母细胞减数分裂对产生正常精细胞和维持基因组稳定性至关重要，且与雄性生育力密切相关，但机制尚不明确。驱动蛋白调控纺锤体微管组装和染色体分离，其研究有助于揭示减数分裂分子机理。前期工作中，我们发现CENP-E抑制导致精母细胞减数分裂染色体排列异常、染色体非整倍性增加和精子发生异常。本项目拟研究CENP-E蛋白在精母细胞减数分裂动粒-微管结合、染色体排列和纺锤体组装检验点调控的作用、动力学和机制，揭示中后期转换点CENP-E蛋白与动粒蛋白在精母细胞纺锤体组装检验点的关键分子链，揭示低浓度GSK923295抑制促进细胞分裂逃逸和逃避检验点的机制，阐明CENP-E蛋白在精母细胞生长分裂和周期调控的双重作用。本项目有助于揭示精母细胞减数分裂和染色体稳定性维持的基本规律和分子机制。

Meiosis of spermatocytes is essential for the production of normal spermatids and maintenance of genomic stability, and is related to male fertility, but the mechanisms remain unknown. Kinesin motors regulate spindle assembly and chromosome segregation, which are helpful to reveal molecular mechanisms of meiosis. In our previous studies, we found that CENP-E inhibition resulted in meiotic chromosome misalignment, increased aneuploidy, and abnormal sperms. This project aims to study the roles, dynamics, and mechanisms of CENP-E in spermatocyte meiotic kinetochore-microtubule attachment, chromosome alignment, and spindle assembly checkpoint. This project is intended to reveal molecular pathways of CENP-E and kinetochore proteins in the spindle assembly checkpoint, and the mechanisms of low concentration GSK923295 inhibition results in the stimulation of cell division and the checkpoint slippage. We seek to clarify the dual roles of CENP-E in cell division and cell cycle regulation in spermatocytes. This project would reveal basic laws and molecular mechanisms of meiosis and the maintenance of chromosomal stability.