TACC3是有丝分裂中重要的纺锤体稳定和组织蛋白，位于中心体，但TACC3调控减数分裂的机制仍未阐明。我们以小鼠卵母细胞为模型，研究了TACC3调节减数分裂的机制，前期结果表明：在GVBD、MI、ATI和MII期，TACC3分布于纺锤体极和星状体，与γ-Tubulin共定位；降调TACC3，导致纺锤体和染色体异常、纺锤体极蛋白γ-Tubulin脱落、第一极体排出率下降和出现大极体；因此推测，TACC3是调控减数分裂的关键蛋白。本项目将利用体外TACC3-mRNA过表达、卵母细胞TACC3特异性基因敲除TACC3F/FGDF9-Cre模型小鼠，探讨TACC3精确调控卵母细胞减数分裂正确有序发生的分子机制。为辅助生殖技术的完善以及卵子发生异常相关疾病的诊治提供理论基础。

TACC3，a member of the human transforming acidic coiled-coil (TACC) protein family，acts as a centrosome protein and is involved in the regulation of spindle assembly in mitosis; however, whether it participates in meiosis remains unclear. We have investigated its localization and function in mouse oocytes, found TACC3 associated with spindle pole and aster, and co-locolized with γ-Tubulin. Down-regulation of TACC3 would result in severe chromosome misalignment, spindle disruption, impaired localization of γ-Tubulin, a decrease in the first polar body extrusion rate and large polar body formation. Collectively, these data demonstrate that TACC3 is required for spindle organization in oocyte meiosis. In this project, we would establish TACC3 over-expression and TACC3F/FGDF9-Cre knockout mouse oocyte model and study the underlying mechanism that how TACC3 regulates oocyte meiosis. This research would improve the theoretical foundation for the treatment of the diseases regarding decreased oocyte quality and the development of assisted reproductive technology.