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Polo样激酶1在小鼠卵母细胞减数分裂过程中参与MEK1/2调节的纺锤体形成。

Involvement of Polo-like kinase 1 in MEK1/2-regulated spindle formation during mouse oocyte meiosis.

作者信息

Xiong Bo, Sun Shao-Chen, Lin Sheng-Li, Li Mo, Xu Bao-Zeng, OuYang Ying-Chun, Hou Yi, Chen Da-Yuan, Sun Qing-Yuan

机构信息

State Key Laboratory of Reproductive Biology, Institute of Zoology and Graduate School, Chinese Academy of Sciences, Beijing, China.

出版信息

Cell Cycle. 2008 Jun 15;7(12):1804-9. doi: 10.4161/cc.7.12.6019. Epub 2008 Jun 26.

Abstract

Our recent studies have shown that MEK1/2 is a critical regulator of microtubule organization and spindle formation during oocyte meiosis. In the present study, we found that Plk1 colocalized with p-MEK1/2 at various meiotic stages after GVBD when microtubule began to organize. Also, Plk1 was able to coimmunoprecipitate with p-MEK1/2 in metaphase I stage mouse oocyte extracts, further confirming their physical interaction. Taxol-treated oocytes exhibited a number of cytoplasmic asters, in which both Plk1 and p-MEK1/2 were present, indicating that they might be complexed to participate in the acentrosomal spindle formation at the MTOCs during oocyte meiosis. Depolymerization of microtubules by nocodazole resulted in the complete disassembly of spindles, but Plk1 remained associated with p-MEK1/2, accumulating in the vicinity of chromosomes. More importantly, when p-MEK1/2 activity was blocked by U0126, Plk1 lost its normal localization at the spindle poles, which might be one of the most vital factors causing the abnormal spindles in MEK1/2-inhibited oocytes. Taken together, these data indicate that Plk1 and MEK1/2 regulate the spindle formation in the same pathway and that Plk1 is involved in MEK1/2-regulated spindle assembly during mouse oocyte meiotic maturation.

摘要

我们最近的研究表明,MEK1/2是卵母细胞减数分裂过程中微管组织和纺锤体形成的关键调节因子。在本研究中,我们发现,在GVBD后微管开始组织的各个减数分裂阶段,Plk1与p-MEK1/2共定位。此外,在中期I期小鼠卵母细胞提取物中,Plk1能够与p-MEK1/2进行免疫共沉淀,进一步证实了它们的物理相互作用。紫杉醇处理的卵母细胞表现出许多胞质星体,Plk1和p-MEK1/2均存在于其中,这表明它们可能形成复合物,参与卵母细胞减数分裂过程中MTOCs处无中心体纺锤体的形成。诺考达唑使微管解聚导致纺锤体完全解体,但Plk1仍与p-MEK1/2相关联,在染色体附近积累。更重要的是,当p-MEK1/2活性被U0126阻断时,Plk1在纺锤体极失去其正常定位,这可能是导致MEK1/2抑制的卵母细胞中纺锤体异常的最重要因素之一。综上所述,这些数据表明Plk1和MEK1/2在同一途径中调节纺锤体形成,并且Plk1参与小鼠卵母细胞减数分裂成熟过程中MEK1/2调节的纺锤体组装。

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