DISRUPTION OF C-MOS CAUSES PARTHENOGENETIC DEVELOPMENT OF UNFERTILIZED MOUSE EGGS
DISRUPTION OF C-MOS CAUSES PARTHENOGENETIC DEVELOPMENT OF UNFERTILIZED MOUSE EGGS
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DOI：
10.1038/370065a0
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发表时间：
1994-07-07
期刊：
影响因子：
64.8
通讯作者：
EVANS, MJ
中科院分区：
文献类型：
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作者：
COLLEDGE, WH;CARLTON, MBL;EVANS, MJ
c-mos原癌基因编码一个37-39K的细胞质丝氨酸/苏氨酸激酶(1)，参与小鼠精子发生(2)和卵子发生（3-6）过程中的减数分裂成熟事件。在非洲爪蟾中，pp39（mos）的异位表达既可以促进卵母细胞的减数分裂成熟（7-9），也可以阻止卵裂球的分裂（10）。为了阐明pp39（mos）的作用，我们在胚胎干细胞中通过基因靶向产生了纯合突变小鼠（11）。这些小鼠是可存活的，突变的雄性小鼠是可生育的，这表明pp39（mos）对精子发生不是必需的。相反，由于成熟卵子在减数分裂期间未能停止，突变雌性的生育能力降低。C-mos（-1-）卵母细胞经历生发囊泡破裂和两极体挤压，在某些情况下进入卵裂。突变的雌性也会产生卵巢囊肿。这些结果表明，pp39（mos）的主要作用是防止未受精卵的自发孤雌生殖激活。
THE c-mos proto-oncogene encodes a 37-39K cytoplasmic serine/threonine kinase(1) implicated in the meiotic maturation events during murine spermatogenesis(2) and oogenesis(3-6). In Xenopus, ectopic expression of pp39(mos) can promote both the meiotic maturation of oocytes(7-9) and also arrest the cleavage of blastomeres(10) To elucidate the role of pp39(mos) we have generated homozygous mutant mice by gene targeting in embryonic stem cells(11). These mice are viable and mutant males are fertile, demonstrating that pp39(mos) is not essential for spermatogenesis. In contrast, mutant females, have a reduced fertility because of the failure of mature eggs to arrest during meiosis. c-mos(-1-) oocytes undergo germinal vesicle breakdown and extrusion of both polar bodies followed in some cases by progression into cleavage. Mutant females also develop ovarian cysts. These results demonstrate that a major role for pp39(mos) is to prevent the spontaneous parthenogenetic activation of unfertilized eggs.