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海星卵母细胞中M期的初始触发:除cdc2激酶外,成熟促进因子的一种可能的新成分。

Initial triggering of M-phase in starfish oocytes: a possible novel component of maturation-promoting factor besides cdc2 kinase.

作者信息

Okumura E, Sekiai T, Hisanaga S, Tachibana K, Kishimoto T

机构信息

Laboratory of Cell and Developmental Biology, Faculty of Biosciences, Tokyo Institute of Technology, Yokohama, Japan.

出版信息

J Cell Biol. 1996 Jan;132(1-2):125-35. doi: 10.1083/jcb.132.1.125.

Abstract

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.

摘要

处于G2期阻滞的未成熟海星卵母细胞含有无活性的cdc2激酶和cdc25磷酸酶,以及一种cdc2激酶的失活剂。在这个系统中,我们研究了调节平衡是如何朝着cdc2激酶的初始激活方向转变的。在激素依赖期(Guerrier, P.和M. Doree,1975年。《发育生物学》47:341 - 348),p34cdc2和cdc25蛋白虽然没有完全转化,但已经部分转化为活性形式,而如果去除激素,cdc2激酶和cdc25磷酸酶的失活剂就能够发挥其活性。我们制备了“触发卵母细胞”,在其中,由于一种中和性抗cdc25抗体,cdc2激酶的激活被阻止,但cdc25蛋白在成熟诱导激素刺激后会轻微磷酸化。与对照未成熟卵母细胞相比,在触发卵母细胞中,注入的cdc2激酶不会失活,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不依赖cdc2激酶活性的过程,该过程抑制cdc2激酶的失活剂并最初使cdc25蛋白磷酸化,尽管这个过程在cdc2激酶的初始激活过程中是可逆的。在M期最开始的触发阶段,不依赖cdc2激酶活性的过程可能会触发导致cdc2激酶初始激活的开关。此后,同时,其他人描述的依赖cdc2激酶的反馈环可能会导致cdc2激酶活性进一步增加。我们提出,一种假定的抑制剂,它独立于核成分下调cdc2激酶的失活剂,可能是成熟促进因子中一个以前未被认识的成分。

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