Interplay between Cdc2 kinase and the c-Mos/MAPK pathway between metaphase I and metaphase II in Xenopus oocytes
Interplay between Cdc2 kinase and the c-Mos/MAPK pathway between metaphase I and metaphase II in Xenopus oocytes
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DOI：
10.1006/dbio.2000.0142
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发表时间：
2001-03-01
影响因子：
2.7
通讯作者：
Jessus, C
中科院分区：
文献类型：
--
作者：
Frank-Vaillant, M;Haccard, O;Jessus, C
爪蟾卵母细胞逮捕在前期我恢复减数分裂响应孕酮和逮捕中期II。进入减数分裂I依赖于Cdc2激酶[M期促进因子（MPF）]的激活。为了更好地理解Cdc2的作用，MPF活性通过注射CDK抑制剂Cip1而被特异性抑制。当Cip1在生殖器囊泡破裂（GVBD）时间注射时，Cdc25和Plx1都去磷酸化，Cdc2在酪氨酸上重新磷酸化。因此，表征MPF的自动扩增环不仅是GVBD之前MPF生成所需的，而且是其在GVBD期间的稳定性所需的。泛素连接酶后期促进复合物/细胞周期体（APC/C），负责细胞周期蛋白降解，也是Cdc2的控制下，因此，Cdc2活性本身诱导其自身的失活通过细胞周期蛋白降解，允许退出第一次减数分裂。相反，细胞周期蛋白的积累，负责Cdc2活性增加，允许进入中期II，是独立的Cdc2。当Cdc2活性在GVBD时被抑制时，c-Mos/丝裂原活化蛋白激酶（MAPK）途径仍然活跃。这条通路可能是负责持续的细胞周期蛋白新合成。相反，在中期II块，c-Mos/MAPK通路依赖于Cdc2。因此，中期II阻滞依赖于MPF和CSF之间的动态相互作用，c-Mos/MAPK途径稳定细胞周期蛋白B，而反过来，MPF阻止c-Mos降解。
Xenopus oocytes arrested in prophase I resume meiotic division in response to progesterone and arrest at metaphase II. Entry into meiosis I depends on the activation of Cdc2 kinase [M-phase promoting factor (MPF)]. To better understand the role of Cdc2, MPF activity was specifically inhibited by injection of the CDK inhibitor, Cip1. When Cip1 is injected at germinal vesicle breakdown (GVBD) time, Cdc25 and Plx1 are both dephosphorylated and Cdc2 is rephosphorylated on tyrosine. The autoamplification loop characterizing MPF is therefore not only required for MPF generation before GVBD, but also for its stability during the GVBD period. The ubiquitine ligase anaphase-promoting complex/cyclosome (APC/C), responsible for cyclin degradation, is also under the control of Cdc2; therefore, Cdc2 activity itself induces its own inactivation through cyclin degradation, allowing the exit from the first meiotic division. In contrast, cyclin accumulation, responsible for Cdc2 activity increase allowing entry into metaphase II, is independent of Cdc2. The c-Mos/mitogen-activated protein kinase (MAPK) pathway remains active when Cdc2 activity is inhibited at GVBD time. This pathway could be responsible for the sustained cyclin neosynthesis. In contrast, during the metaphase II block, the c-Mos/MAPK pathway depends on Cdc2. Therefore, the metaphase II block depends on a dynamic interplay between MPF and CSF, the c-Mos/MAPK pathway stabilizing cyclin B, whereas in turn, MPF prevents c-Mos degradation.