Role of Greatwall kinase in release of mouse oocytes from diplotene arrest. (4th December 2014)

• Record Type: Journal Article
• Authors: Zhao, Xiangyu; Yu, Dahai; Feng, Chen; Deng, Xin; Wu, Didi; Jin, Minglin; Wang, Enhua; Wang, Xiuxia; Yu, Bingzhi
• Is Part Of: Development growth and differentiation. Volume 56:Number 9(2014)
• Page Start: 669
• Page End: 678
• Publication Date: 2014-12-04
• Subjects: Embryology -- Periodicals; Developmental biology -- Periodicals; Growth -- Periodicals; 574.3
• DOI: 10.1111/dgd.12183
• Languages: English
• ISSNs: 0012-1592

Abstract

<abstract abstract-type="main" id="dgd12183-abs-0001"> <title> <x xml:space="preserve">Abstract</x> </title> <p>In eukaryotes, mitosis entry is induced by activation of maturation‐promoting factor (MPF), which is regulated by a network of kinases and phosphatases. It has been suggested that Greatwall (GWL) kinase was crucial for the M‐phase entry and could maintain cyclin B–Cdc2 activity through regulation of protein phosphatase 2A (PP2A), a counteracting phosphatase of MPF. Here, the role of GWL was assessed during release of mouse oocytes from prophase I arrest. GWL was crucial for meiotic maturation in mouse oocytes. As a positive regulator for meiosis resumption, GWL was continually expressed in germinal vesicle (GV) and MII stage oocytes and two‐cell stage embryos. Additionally, GWL localized to the nucleus and dispersed into cytoplasm during GV breakdown (GVBD). Furthermore, downregulation of GWL or overexpression of catalytically‐inactive GWL inhibited partial meiotic maturation. This prophase I arrest induced by GWL depletion could be rescued by the PP2A inhibition. However, both GWL‐depleted and rescued oocytes had severe spindle defects that hardly reached MII. In contrast, oocytes overexpressing wild‐type GWL resumed meiosis and progressed to MII stage. Thus, our data demonstrate that GWL acts in a pathway with PP2A which is essential for prophase I exit and metaphase I microtubule assembly in mouse oocytes.</p> </abstract>