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首页> 外文期刊>Molecular reproduction and development >Mitogen activated protein kinase plays a significant role in metaphase II arrest, spindle morphology, and maintenance of maturation promoting factor activity in bovine oocytes.
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Mitogen activated protein kinase plays a significant role in metaphase II arrest, spindle morphology, and maintenance of maturation promoting factor activity in bovine oocytes.

机译：丝裂原活化的蛋白激酶在牛卵母细胞的II期中期停滞，纺锤体形态和维持成熟促进因子活性中起着重要作用。

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摘要

Mammalian oocytes are arrested at the G2/M transition of the first meiotic division from which, after reaching full size and subsequent to an LH surge, they undergo final maturation. Oocyte maturation, which involves germinal vesicle breakdown, progression through metaphase I (MI), and arrest at MII, is triggered and regulated by the coordinated action of two kinases, maturation promoting factor (MPF) and mitogen activated protein kinase (MAPK). The importance of the role of MPF in mammalian oocyte maturation is well established, while the role of MAPK, although well understood in mouse oocytes, has not been fully elucidated in oocytes of large domestic species, especially bovine oocytes. Here we show that injection of MKP-1 mRNA, which encodes a dual specificity MAPK phosphatase, into germinal vesicle stage bovine oocytes prevents the activation of MAPK during maturation. Despite the lack of MAPK activity, MKP-1-injected oocytes resume and progress through meiosis, although they are unable to arrest at MII stage and, by 22-26-hour post-maturation, exhibit decondensed pronucleus-like chromatin, a clear sign of parthenogenetic activation. MKP-1-injected bovine oocytes exhibit normal activation of MPF activity; however, by 18-hour post-maturation, MPF activity starts to decline and by 22-26 hr MPF activity is absent. MKP-1-injected oocytes also show disorganized MII spindles with poorly aligned chromosomes. In summary, our results demonstrate that in bovine oocytes MAPK activity is required for MII arrest, maintenance of MPF activity, and spindle organization. Copyright 2001 Wiley-Liss, Inc.
机译：哺乳动物卵母细胞停滞在第一个减数分裂的G2 / M过渡期，在达到最大大小后并在LH激增后，它们经历了最终的成熟。卵母细胞的成熟涉及生发囊泡的破坏，通过中期I（MI）的进展以及在MII的停滞，这是由两种激酶（成熟促进因子（MPF）和促分裂原活化蛋白激酶（MAPK））的协同作用触发和调节的。众所周知，MPF在哺乳动物卵母细胞成熟中的作用很重要，而MAPK的作用虽然在小鼠卵母细胞中已广为人知，但在大型家养卵母细胞（尤其是牛卵母细胞）中尚未得到充分阐明。在这里，我们表明向生小泡期牛卵母细胞注射编码双重特异性MAPK磷酸酶的MKP-1 mRNA可防止MAPK在成熟过程中激活。尽管缺乏MAPK活性，但注射MKP-1的卵母细胞虽然无法在MII阶段停滞，并且在成熟后22-26小时显示出脱核的核样染色质，但仍能通过减数分裂恢复和发展。孤雌激活。注射了MKP-1的牛卵母细胞显示出MPF活性的正常激活。但是，到成熟后18小时，MPF活性开始下降，到22-26小时，MPF活性消失。注射了MKP-1的卵母细胞还显示出杂乱无章的MII纺锤体，其染色体排列不佳。总之，我们的结果表明，在牛卵母细胞中，MAPK活性是MII阻滞，维持MPF活性和纺锤体组织所必需的。版权所有2001 Wiley-Liss，Inc.

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