Abrieu A, Dorée M, Picard A
Laboratoire Arago, Banyuls-sur-Mer, France.
Mol Biol Cell. 1997 Feb;8(2):249-61. doi: 10.1091/mbc.8.2.249.
The G2 arrest of oocytes from frogs, clams, and starfish requires that preformed cyclin B-cdc2 complexes [prematuration-promoting factor (MPF)] be kept in an inactive form that is largely due to inhibitory phosphorylation of this pre-MPF. We have investigated the role of mitogen-activated protein (MAP) kinase in the activation of this pre-MPF. The cytoplasm of both frog and starfish oocytes contains an activity that can rapidly inactivate injected MPF. When the MAP kinase of G2-arrested starfish or Xenopus oocytes was prematurely activated by microinjection of c-mos or Ste-11 delta N fusion proteins, the rate and extent of MPF inactivation was much reduced. Both effects were suppressed by expression of the specific MAP kinase phosphatase Pyst 1. These results show that MAP kinase down-regulates a mechanism that inactivates cyclin B-cdc2 kinase in Xenopus oocytes. In starfish oocytes, however, MAP kinase activation occurs only after germinal vesicle breakdown, much after MPF activation. In this case, down-regulation of the cyclin B-cdc2 inhibiting pathway is a sensitive response to hormonal stimulation that does not require MAP kinase activation.
青蛙、蛤蜊和海星卵母细胞的G2期阻滞要求预先形成的细胞周期蛋白B - cdc2复合物[促成熟因子（MPF）]保持无活性状态，这主要归因于该前体MPF的抑制性磷酸化。我们研究了丝裂原活化蛋白（MAP）激酶在该前体MPF激活过程中的作用。青蛙和海星卵母细胞的细胞质中都有一种活性物质，它能迅速使注入的MPF失活。当通过显微注射c - mos或Ste - 11δN融合蛋白过早激活处于G2期阻滞的海星或非洲爪蟾卵母细胞的MAP激酶时，MPF失活的速率和程度会大大降低。这两种效应都被特异性MAP激酶磷酸酶Pyst 1的表达所抑制。这些结果表明，MAP激酶下调了非洲爪蟾卵母细胞中使细胞周期蛋白B - cdc2激酶失活的一种机制。然而，在海星卵母细胞中，MAP激酶的激活仅在生发泡破裂后发生，远在MPF激活之后。在这种情况下，细胞周期蛋白B - cdc2抑制途径的下调是对激素刺激的一种敏感反应，并不需要MAP激酶的激活。
