Deparment of Animal Sciences, Chungbuk National University, Korea.
Cell Cycle. 2010 Nov 15;9(22):4552-9. doi: 10.4161/cc.9.22.13815.
Spc25 is a component of the Ndc80 complex which consists of Ndc80, Nuf2, Spc24, and Spc25. Previous work has shown that Spc25 is involved in regulation of kinetochore microtubule attachment and the spindle assembly checkpoint in mitosis. The roles of Spc25 in meiosis remain unknown. Here, we report its expression, localization and functions in mouse oocyte meiosis. The Spc25 mRNA level gradually increased from the GV to MI stage, but decreased by MII during mouse oocyte meiotic maturation. Immunofluorescent staining showed that Spc25 was restricted to the germinal vesicle, and associated with chromosomes during all stages after GVBD. Overexpression of Spc25 by mRNA injection resulted in oocyte meiotic arrest, chromosome misalignment and spindle disruption. Conversely, Spc25 RNAi by siRNA injection resulted in precocious polar body extrusion and caused severe chromosome misalignment and aberrant spindle formation. Our data suggest that Spc25 is required for chromosome alignment, spindle formation, and proper spindle checkpoint signaling during meiosis.
Spc25 是 Ndc80 复合物的一个组成部分,该复合物由 Ndc80、Nuf2、Spc24 和 Spc25 组成。之前的工作表明 Spc25 参与调节有丝分裂中的动粒微管附着和纺锤体组装检查点。Spc25 在减数分裂中的作用尚不清楚。在这里,我们报告了它在小鼠卵母细胞减数分裂中的表达、定位和功能。Spc25 mRNA 水平从 GV 期逐渐增加到 MI 期,但在小鼠卵母细胞减数分裂成熟过程中在 MII 期下降。免疫荧光染色显示 Spc25 局限于生发泡,并且在 GVBD 后所有阶段与染色体相关。通过 mRNA 注射过表达 Spc25 导致卵母细胞减数分裂停滞、染色体错位和纺锤体解体。相反,通过 siRNA 注射 Spc25 RNAi 导致过早的极体排出,并导致严重的染色体错位和异常纺锤体形成。我们的数据表明 Spc25 是减数分裂过程中染色体排列、纺锤体形成和适当的纺锤体检查点信号所必需的。