Initial triggering of M-phase in starfish oocytes: a possible novel component of maturation-promoting factor besides cdc2 kinase.
Initial triggering of M-phase in starfish oocytes: a possible novel component of maturation-promoting factor besides cdc2 kinase.
复制标题
DOI：
10.1083/jcb.132.1.125
复制
发表时间：
1996-01
期刊：
影响因子：
--
通讯作者：
Kishimoto T
中科院分区：
文献类型：
--
作者：
Okumura E;Sekiai T;Hisanaga S;Tachibana K;Kishimoto T
g2期阻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激酶的失活因子。在这个系统中，我们已经研究了调节平衡是如何作用于cdc2激酶的初始激活的。在激素依赖期（Guerrier， P., and M. Doree, 1975）。开发生物学。47:341-348)，p34cdc2和cdc25蛋白已经转化为活性形式，尽管不完全，然而cdc2激酶和cdc25磷酸酶的失活因子能够在激素被移除时显示其活性。我们制造了“触发卵母细胞”，其中由于中和的抗dc25抗体，cdc2激酶的激活被阻止，cdc25蛋白在诱导成熟的激素刺激后被轻微磷酸化。与未成熟卵母细胞相比，在触发卵母细胞中，注射的cdc2激酶不会失活，因此减数分裂再起始所需的cdc2激酶活性水平要低得多。这些结果暗示cdc2激酶活性独立过程的存在，该过程抑制cdc2激酶的失活因子并最初使cdc25蛋白磷酸化，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激酶活性无关的过程可能会触发导致cdc2激酶初始激活的开关。此后，类似地，其他人描述的cdc2激酶依赖的反馈回路可能导致cdc2激酶活性进一步增加。我们提出一个假定的抑制因子，它可以独立于核成分下调cdc2激酶的失活因子，可能是一个以前未被识别的成熟促进因子的成分。
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.