Symmetry breaking in mouse oocytes requires transient F-actin meshwork destabilization
Symmetry breaking in mouse oocytes requires transient F-actin meshwork destabilization
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DOI：
10.1242/dev.060269
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发表时间：
2011-07-15
期刊：
影响因子：
4.6
通讯作者：
Verlhac, Marie-Helene
中科院分区：
文献类型：
--
作者：
Azoury, Jessica;Lee, Karen Wingman;Verlhac, Marie-Helene
雌性减数分裂是极不对称的，产生一个大的卵母细胞和小的退化极体，为进一步的胚胎发育保留母体储备。这种不对称性是通过分度轴的偏心定位实现的。小鼠卵母细胞已经开发出一种基于肌动蛋白的纺锤体定位机制，该机制允许减数分裂纺锤体向最近的皮质迁移。利用旋转圆盘显微镜和FRAP分析，我们研究了在第一次减数分裂的细胞质F-肌动蛋白网络的组织的变化。它在前期I是非常密集的，在减数分裂恢复后经历了一个显着的密度下降，并在以后进行性改革。在减数分裂I进入时高水平的β 2诱导网络维持，导致施加在染色体上的力相等，防止纺锤体迁移。因此，减数分裂恢复时的网络密度下降与成功的不对称减数分裂所需的破环事件密切相关。
Female meiotic divisions are extremely asymmetric, giving rise to a large oocyte and small degenerating polar bodies, keeping the maternal stores for further embryo development. This asymmetry is achieved via off-center positioning of the division spindle. Mouse oocytes have developed a formin-2-dependent actin-based spindle positioning mechanism that allows the meiotic spindle to migrate towards the closest cortex. Using spinning disk microscopy and FRAP analysis, we studied the changes in the organization of the cytoplasmic F-actin meshwork during the first meiotic division. It is very dense in prophase I, undergoes a significant density drop upon meiosis resumption and reforms progressively later on. This meshwork remodeling correlates with endogenous formin 2 regulation. High formin 2 levels at meiosis I entry induce meshwork maintenance, leading to equal forces being exerted on the chromosomes, preventing spindle migration. Hence, the meshwork density drop at meiosis resumption is germane to the symmetry-breaking event required for successful asymmetric meiotic divisions.