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非洲爪蟾卵母细胞成熟过程中Mos原癌基因的功能

Mos proto-oncogene function during oocyte maturation in Xenopus.

作者信息

Roy L M, Haccard O, Izumi T, Lattes B G, Lewellyn A L, Maller J L

机构信息

Howard Hughes Medical Institute, University of Colorado School of Medicine, Denver, 80262, USA.

出版信息

Oncogene. 1996 May 16;12(10):2203-11.

PMID:8668347
Abstract

The function of the Xenopus c-mos proto-oncogene product (Mos(xe)) has been investigated during oocyte maturation. Experiments with a new antibody able to immunoblot Mos(xe) demonstrated the time course of MAP kinase (MAP K) activation in oocytes paralleled Mos(xe) accumulation, and in activated eggs the deactivation of MAP K paralleled the degradation of Mos(xe). Ablation of Mos synthesis by microinjection of antisense oligodeoxynucleotides abolished activation of MAP K by progesterone, but microinjection of GST-Mos fully restored both MAP K activation and germinal vesicle breakdown (GVBD). The Mos(xe) level at metaphase of Meiosis I (MI) was 2 - 3-fold less than that at metaphase of Meiosis II (MII), but MAP K activation was maximal at metaphase in both MI and MII. In the transition between MI and MII, both cyclin B and Mos(xe) levels rapidly declined in the presence of cycloheximide and injection of exogenous GST-Mos(xe) did not prevent degradation of either protein, although MAP K was activated. Microinjection of GST-Mos(xe) into oocytes was able to activate MAP K before GVBD and H1 kinase activation, and microinjection of constitutively-activated thiophosphorylated MAP K induced de novo synthesis of Mos(xe) before H1 kinase activation, suggesting the existence of a positive feedback loop between MAP K and Mos(xe) accumulation.

摘要

非洲爪蟾c-mos原癌基因产物(Mos(xe))的功能在卵母细胞成熟过程中得到了研究。使用一种能够对Mos(xe)进行免疫印迹的新抗体所做的实验表明,卵母细胞中丝裂原活化蛋白激酶(MAP激酶,MAP K)的激活时间进程与Mos(xe)的积累平行,而在激活的卵中,MAP K的失活与Mos(xe)的降解平行。通过显微注射反义寡脱氧核苷酸消除Mos的合成,消除了孕酮对MAP K的激活,但显微注射GST-Mos完全恢复了MAP K的激活和生发泡破裂(GVBD)。减数分裂I(MI)中期的Mos(xe)水平比减数分裂II(MII)中期低2 - 3倍,但在MI和MII中期MAP K的激活均达到最大值。在MI和MII的转换过程中,在存在环己酰亚胺的情况下,细胞周期蛋白B和Mos(xe)水平均迅速下降,并且注射外源GST-Mos(xe)并不能阻止这两种蛋白质的降解,尽管MAP K被激活。向卵母细胞中显微注射GST-Mos(xe)能够在GVBD和H1激酶激活之前激活MAP K,而向卵母细胞中显微注射组成型激活的硫代磷酸化MAP K能够在H1激酶激活之前诱导Mos(xe)的从头合成,这表明在MAP K和Mos(xe)积累之间存在正反馈环。

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