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C-MOS FORCES THE MITOTIC CELL CYCLE TO UNDERGO MEIOSIS II TO PRODUCE HAPLOID GAMATES

C-MOS 迫使有丝分裂细胞周期经历减数分裂 II 以产生单倍体配子

基本信息

批准号：
11680717
负责人：
TACHIBANA Kazunori
金额：
$ 2.24万
依托单位：
Tokyo Institute of Technology
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1999
资助国家：
日本
起止时间：
1999 至 2000
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-11680717/
关键词：
c-Mos MAP kinase activation DNA replication oocyte maturation meiosis cell cycle parthenogenesis MOS

项目摘要

We have studied the functions of c-Mos proto oncogene product in starfish oocyte maturation and early embryonic cell cycles. The meiotic cycle reduces ploidy through two consecutive M phases, meiosis I and meiosis II, without an intervening S phase. To maintain ploidy through successive generations, meiosis must be followed by mitosis after the recovery of diploidy by fertilization. However, the coordination from meiotic to mitotic cycle is still unclear. Mos, the c-mos protooncogene product, is a key regulator of meiosis in vertebrates. In contrast to the previous observation that Mos, functions only in vertebrate oocytes that arrest at meiotic metaphase II, here we isolate the first invertebrate mos from starfish and show that Mos functions also in starfish oocytes that arrest after the completion of meiosis II but not at metaphase II.In the absence of Mos meiosis I is followed directly by repeated embryonic mitotic cycles, and its reinstatement restores meiosis II and subsequent cell cycle arrest. These observations imply that after meiosis I, oocytes have a competence to progress through the embryonic mitotic cycle, but that Mos diverts the cell cycle to execute meiosis II and remains to restrain the return to the mitotic cycle. We propose that a role of Mos that is conserved in invertebrate and vertebrate oocytes is not to support metaphase II arrest but to prevent the meiotic/mitotic conversion after meiosis I until fertilization, directing meiosis II to ensure the reduction of ploidy.

我们研究了c-mos原癌基因产物在海星卵母细胞成熟和早期胚胎细胞周期中的作用。减数分裂周期通过两个连续的M期来减少倍性，减数分裂I和减数分裂II，没有S的介入。为了在后代中保持倍性，减数分裂必须在二倍体通过受精恢复后进行有丝分裂。然而，从减数分裂到有丝分裂周期的协调仍然不清楚。MOS是原癌基因c-mos的产物，是脊椎动物减数分裂的关键调控因子。与以前的观察结果不同的是，MOS仅在减数分裂中期II停滞的脊椎动物卵母细胞中起作用，这里我们从海星中分离出第一批无脊椎动物MOS，并表明MOS在海星卵母细胞中也起作用，这些卵母细胞在减数分裂II完成后停止，但在中期II不起作用。这些观察结果表明，在减数分裂I之后，卵母细胞具有通过胚胎有丝分裂周期的能力，但MOS将细胞周期转移到执行减数分裂II，并继续抑制回到有丝分裂周期。我们认为，在无脊椎动物和脊椎动物卵母细胞中保守的MOS的作用不是支持中期II的停滞，而是阻止减数分裂I之后的减数分裂/有丝分裂转换，直到受精，指导减数分裂II以确保倍性的减少。