The Mos/MAPK pathway is involved in metaphase II arrest as a cytostatic factor but is neither necessary nor sufficient for initiating oocyte maturation in goldfish

The Mos/MAPK pathway is involved in metaphase II arrest as a cytostatic factor but is neither necessary nor sufficient for initiating oocyte maturation in goldfish
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DOI:
10.1007/s004270000083
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发表时间:
2000-09-01
影响因子:
2.4
通讯作者:
Nagahama, Y
Nagahama, Y
中科院分区:
生物学4区
文献类型:
--
作者:
Kajiura-Kobayashi, H;Yoshida, N;Nagahama, Y

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MOS在脊椎动物减数分裂过程中起着至关重要的作用。在非洲爪哇,MOS作为启动因子参与了卵母细胞成熟的启动,作为细胞抑制因子(CSF)的一部分参与了中期II期(MII)的停滞。MOS的功能由MAPK(MAPK)介导。我们研究了MOS/MAPK通路在17α,20β-二羟基-4-孕烯-3-酮(17α,20β-DP)诱导金鱼卵母细胞成熟过程中的作用。未成熟的金鱼卵母细胞中不存在MOS。它在生发泡破裂(GVBD)发生前就开始出现,在MII停滞的成熟卵母细胞中达到最大值,受精后消失。MAPK在MOS合成后激活,但在成熟促进因子(MPF)激活之前激活,在MII时活性达到最大。将非洲爪哇和金鱼c-mos基因分别注入非洲爪哇和金鱼2-细胞期胚胎的一个卵裂球内,均可引起中期分裂停滞,提示金鱼MOS具有脑脊液活性。在未成熟的金鱼卵母细胞中注射具有结构性活性的非洲爪哇c-mos m RNA可诱导MAPK激活,但不能激活MPF和GVBD。相反,注射金鱼c-mos反义RNA可抑制17α、20β-DP处理的卵母细胞的MOS合成和MAPK激活,但这些卵母细胞经历了GVBD。这些结果表明,尽管MOS/MAPK途径具有脑脊液的一般功能,但它并不是启动金鱼卵母细胞成熟所必需的。结合未成熟卵母细胞中储存的非活性MPF(前MPF)含量的差异,讨论了MOS/MAPK在卵母细胞成熟过程中的一般作用。
Mos plays a crucial role in meiotic cell division in vertebrates. In Xenopus, Mos is involved in the initiation of oocyte maturation as an initiator and in the arrest at the metaphase II stage (MII) as a component of the cytostatic factor (CSF. The function of Mos is mediated by MAP kinase (MAPK). We investigated the function of the Mos/MAPK pathway during goldfish oocyte maturation induced by 17 alpha,20 beta-dihydroxy-4-pregnen-3-one (17 alpha,20 beta-DP), a natural maturation-inducing hormone in fishes. Mos was absent in immature goldfish oocytes. It appeared before the onset of germinal vesicle breakdown (GVBD), increased to a maximum in mature oocytes arrested at MII and disappeared after fertilization. MAPK was activated after Mos synthesis but before maturation-promoting factor (MPF) activation, and its activity reached maximum at MII. Injection of either Xenopus or goldfish c-mos mRNA into one blastomere of 2-cell-stage Xenopus and goldfish embryos induced metaphase arrest, suggesting that goldfish Mos has a CSF activity. Injection of constitutively active Xenopus c-mos mRNA into immature goldfish oocytes induced MAPK activation, but neither MPF activation nor GVBD occurred. Conversely, the injection of goldfish c-mos antisense RNA inhibited both Mos synthesis and MAPK activation in the 17 alpha,20 beta-DP-treated oocytes, but these oocytes underwent GVBD. These results indicate that the Mos/MAPK pathway is not essential For initiating goldfish oocyte maturation despite its general function as a CSF. We discuss the general role of Mos/MAPK during oocyte maturation, with reference to the difference in contents of inactive MPF (pre-MPF) stored in immature oocytes.