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鱼类和两栖类卵母细胞减数分裂成熟与阻滞的分子机制。

Molecular mechanisms of meiotic maturation and arrest in fish and amphibian oocytes.

作者信息

Yamashita M

机构信息

Laboratory of Molecular and Cellular Interactions, Division of Biological Sciences, Graduate School of Science, Hokkaido University, Sapporo, 060-0810, Japan.

出版信息

Semin Cell Dev Biol. 1998 Oct;9(5):569-79. doi: 10.1006/scdb.1998.0251.

Abstract

Fish and amphibian oocytes provide excellent experimental systems for both biochemical and cytological analyses of regulatory mechanisms of meiotic maturation and arrest. Recent work shows that despite the adoption of common players, such as maturation-promoting factor (MPF), c-mos proto-oncogene product (Mos), and mitogen-activated protein kinase (MAPK), there is clear species-specificity in the mechanisms, probably due to the difference in the states of inactive MPF in immature oocytes. However, it has also been revealed that the mechanisms controlling meiotic maturation and arrest include ubiquitous pathways; The translational activation of masked mRNAs encoding Mos and cyclin B for initiating maturation and the Mos-MAPK pathway for maintaining metaphase arrest.

摘要

鱼类和两栖类卵母细胞为减数分裂成熟和阻滞调控机制的生化及细胞学分析提供了出色的实验系统。近期研究表明,尽管采用了诸如成熟促进因子(MPF)、原癌基因c-mos产物(Mos)和丝裂原活化蛋白激酶(MAPK)等共同作用因子,但在机制上仍存在明显的物种特异性,这可能是由于未成熟卵母细胞中无活性MPF状态的差异所致。然而,也有研究揭示,控制减数分裂成熟和阻滞的机制包括普遍存在的途径;编码Mos和细胞周期蛋白B的隐蔽mRNA的翻译激活以启动成熟,以及Mos-MAPK途径以维持中期阻滞。

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