首页> 美国卫生研究院文献>Proceedings of the National Academy of Sciences of the United States of America >Mos/mitogen-activated protein kinase can induce early meiotic phenotypes in the absence of maturation-promoting factor: a novel system for analyzing spindle formation during meiosis I.
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Mos/mitogen-activated protein kinase can induce early meiotic phenotypes in the absence of maturation-promoting factor: a novel system for analyzing spindle formation during meiosis I.

机译:Mos /促分裂原活化蛋白激酶可以在缺乏成熟促进因子的情况下诱导早期减数分裂表型:一种分析减数分裂I期间纺锤体形成的新型系统。

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摘要

Mitogen-activated protein kinase (MAPK) is selectively activated by injecting either mos or MAPK kinase (mek) RNA into immature mouse oocytes maintained in the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX). IBMX arrests oocyte maturation, but Mos (or MEK) overexpression overrides this block. Under these conditions, meiosis I is significantly prolonged, and MAPK becomes fully activated in the absence of p34cdc2 kinase or maturation-promoting factor. In these oocytes, large openings form in the germinal vesicle adjacent to condensing chromatin, and microtubule arrays, which stain for both MAPK and centrosomal proteins, nucleate from these regions. Maturation-promoting factor activation occurs later, concomitant with germinal vesicle breakdown, the contraction of the microtubule arrays into a precursor of the spindle, and the redistribution of the centrosomal proteins into the newly forming spindle poles. These studies define important new functions for the Mos/MAPK cascade in mouse oocyte maturation and, under these conditions, reveal novel detail of the early stages of oocyte meiosis I.
机译:通过将mos或MAPK激酶(mek)RNA注射入磷酸二酯酶抑制剂3-异丁基-1-甲基黄嘌呤(IBMX)中保持的未成熟小鼠卵母细胞中,选择性激活丝裂原活化的蛋白激酶(MAPK)。 IBMX阻止了卵母细胞的成熟,但是Mos(或MEK)的过表达将覆盖此障碍。在这些条件下,减数分裂I显着延长,并且在不存在p34cdc2激酶或成熟促进因子的情况下,MAPK完全活化。在这些卵母细胞中,在生发囊泡中形成一个大的开口,与浓缩的染色质相邻,而对MAPK和中心体蛋白都染色的微管阵列则从这些区域形成核。促进成熟的因子激活发生得较晚,伴随生发囊泡破裂,微管阵列收缩成纺锤体的前体以及中心体蛋白重新分布到新形成的纺锤体极。这些研究为Mos / MAPK级联在小鼠卵母细胞成熟中定义了重要的新功能,并且在这些条件下,揭示了卵母细胞减数分裂I早期的新细节。

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