首页> 美国卫生研究院文献>The Journal of Biophysical and Biochemical Cytology >Initial triggering of M-phase in starfish oocytes: a possible novel component of maturation-promoting factor besides cdc2 kinase
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Initial triggering of M-phase in starfish oocytes: a possible novel component of maturation-promoting factor besides cdc2 kinase

机译:海星卵母细胞M期的初始触发:除了cdc2激酶外可能有成熟促进因子的新成分

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摘要

G2-phase-arrested immature starfish oocytes contain inactive cdc2 kinase and cdc25 phosphatase, and an inactivator for cdc2 kinase. In this system, we have studied how the regulatory balance is apped toward the initial activation of cdc2 kinase. During the hormone-dependent period (Guerrier, P., and M. Doree, 1975. Dev. Biol. 47:341-348), p34cdc2 and cdc25 protein are already converted, though not fully, to active forms, whereas the inactivators for cdc2 kinase and cdc25 phosphatase are able to exhibit their activities if the hormone were removed. We produced "triggered oocytes," in which due to a neutralizing anticdc25 antibody, the activation of cdc2 kinase is prevented out cdc25 protein is phosphorylated slightly after the maturation-inducing hormonal stimulus. In contrast to control immature oocytes, in triggered oocytes the injected cdc2 kinase is not inactivated, and accordingly the level of cdc2 kinase activity required for meiosis reinitiation is much less. These results imply the presence of a cdc2 kinase activity-independent process(es) that suppresses the inactivator for cdc2 kinase and initially phosphorylates cdc25 protein, although this process is reversible during the initial activation of cdc2 kinase. At the most initial triggering of M-phase, the cdc2 kinase activity-independent process might trip the switch leading to the initial activation of cdc2 kinase. Thereafter, in parallel, the cdc2 kinase-dependent feedback loops described by others may cause further increase in cdc2 kinase activity. We propose that a putative suppressor, which downregulates the inactivator for cdc2 kinase independently of nuclear components, might be a previously unrecognized component of maturation-promoting factor.
机译:G2期停滞的未成熟海星卵母细胞含有失活的cdc2激酶和cdc25磷酸酶,以及cdc2激酶的失活剂。在这个系统中,我们研究了调节平衡如何与cdc2激酶的初始激活相适应。在激素依赖性期间(Guerrier,P.和M. Doree,1975. Dev。Biol。47:341-348),p34cdc2和cdc25蛋白已经(尽管不完全)转化为活性形式,而灭活剂如果去除了激素,cdc2激酶和cdc25磷酸酶能够发挥其活性。我们生产了“触发的卵母细胞”,其中由于中和了anticdc25抗体,因此在诱导成熟的激素刺激后,cdc25蛋白被略微磷酸化,从而阻止了cdc2激酶的激活。与对照未成熟卵母细胞相反,在触发的卵母细胞中,注入的cdc2激酶未失活,因此减数分裂重新启动所需的cdc2激酶活性水平要低得多。这些结果表明存在一个cdc2激酶活性独立过程,该过程可抑制cdc2激酶的失活剂并最初磷酸化cdc25蛋白,尽管该过程在cdc2激酶的初始激活过程中是可逆的。在M期的最初始触发时,cdc2激酶活性非依赖性过程可能会使开关跳闸,从而导致cdc2激酶的初始激活。此后,其他人并行描述的cdc2激酶依赖性反馈回路可能会导致cdc2激酶活性进一步提高。我们建议推定的抑制剂,独立于核成分而下调cdc2激酶的失活剂,可能是成熟促进因子的先前未被识别的成分。

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