Control of G2/M transition in Xenopus by a member of the p21-activated kinase (PAK) family:: A link between protein kinase a and PAK signaling pathways?

Control of G2/M transition in Xenopus by a member of the p21-activated kinase (PAK) family:: A link between protein kinase a and PAK signaling pathways?
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DOI:
10.1074/jbc.274.6.3573
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发表时间:
1999-02-05
影响因子:
4.8
通讯作者:
Morin, N
Morin, N
中科院分区:
生物学2区
文献类型:
--
作者:
Faure, S;Vigneron, S;Morin, N

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X-PAKs参与爪蟾卵母细胞成熟过程的负调控(1)。在本研究中,我们更精确地定义了激酶在抑制G(2)/M转换中的靶向事件。我们发现,显微注射重组X-PAK 1-Cter活性激酶到孕酮处理的卵母细胞中阻止了c-Mos的积累和MAPK和促成熟因子(MPF)的激活。在允许MAPK激活的条件下,MPF激活仍然失败。我们证明,组成型截短的X-PAK 1(X-PAK 1-Cter)不会阻止细胞周期蛋白B与p34(cdc 2)的关联,而是阻止卵母细胞中存在的无活性复合物的激活。参与MPF扩增环的蛋白质,包括Cdc 25激活的Polo样激酶都被阻断。实际上,使用活性MPF,在X-PAK 1存在下不打开扩增环。我们的研究结果表明,X-PAK和蛋白激酶A在控制卵母细胞成熟的目标是相似的,此外,这种负调控并不局限于减数分裂,因为我们证明,G(2)/M进程也阻止在爪蟾循环提取物中的活性X-PAK 1的存在。
X-PAKs are involved in negative control of the process of oocyte maturation in Xenopus (1), In the present study, we define more precisely the events targetted by the kinase in the inhibition of the G(2)/M transition. We show that microinjection of recombinant X-PAK1-Cter active kinase into progesterone-treated oocytes prevents c-Mos accumulation and activation of both MAPK and maturation-promoting factor (MPF), In conditions permissive for MAPK activation, MPF activation still fails. We demonstrate that a constitutive truncated version of X-PAK1 (X-PAK1-Cter) does not prevent the association of cyclin B with p34(cdc2) but rather prevents the activation of the inactive complexes present in the oocyte. Proteins participating in the MPF amplification loop, including the Cdc25-activating Polo-like kinase are all blocked. Indeed, using active MPF, the amplification loop is not turned on in the presence of X-PAK1. Our results indicate that X-PAK and protein kinase A targets in the control of oocyte maturation are similar and furthermore that this negative regulation is not restricted to meiosis, because we demonstrate that G(2)/M progression is also prevented in Xenopus cycling extracts in the presence of active X-PAK1.