Full activation of p34CDC28 histone H1 kinase activity is unable to promote entry into mitosis in checkpoint-arrested cells of the yeast Saccharomyces cerevisiae.
Full activation of p34CDC28 histone H1 kinase activity is unable to promote entry into mitosis in checkpoint-arrested cells of the yeast Saccharomyces cerevisiae.
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p34CDC28 组蛋白 H1 激酶活性的完全激活无法促进酿酒酵母检查点停滞细胞进入有丝分裂。
DOI：
10.1128/mcb.13.6.3744-3755.1993
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发表时间：
1993
影响因子：
5.3
通讯作者：
Reed,SI
中科院分区：
文献类型：
--
作者：
Stueland,CS;Lew,DJ;Cismowski,MJ;Reed,SI
在大多数细胞中，有丝分裂依赖于DNA复制的完成。阻止DNA受损或不完全复制的细胞进入有丝分裂的反馈机制被称为检查点控制。对裂殖酵母裂殖酵母和爪蟾卵提取物的研究表明，检查点控制阻止了主调节蛋白激酶p34 cdc 2的激活，该激酶通常触发进入有丝分裂。这是通过抑制p34 cdc 2的Tyr-15残基的磷酸化来实现的。然而，对芽殖酵母Saccharomyces gouae的研究表明，该残基的磷酸化对于阻止有丝分裂的检查点控制并不重要。我们已经调查了在这种生物体的检查点控制的基础，并表明，这些控制可以防止进入有丝分裂，即使在细胞已经完全激活的细胞周期蛋白B（Cl B）相关形式的出芽酵母同源物p34 cdc 2，p34 CDC 28，作为组蛋白H1激酶活性测定。然而，在检查点逮捕的细胞中的活性复合物小于那些在循环细胞，这表明有丝分裂诱导复合物的组装需要额外的步骤后，组蛋白H1激酶激活。
In most cells, mitosis is dependent upon completion of DNA replication. The feedback mechanisms that prevent entry into mitosis by cells with damaged or incompletely replicated DNA have been termed checkpoint controls. Studies with the fission yeast Schizosaccharomyces pombe and Xenopus egg extracts have shown that checkpoint controls prevent activation of the master regulatory protein kinase, p34cdc2, that normally triggers entry into mitosis. This is achieved through inhibitory phosphorylation of the Tyr-15 residue of p34cdc2. However, studies with the budding yeastSaccharomyces cerevisiaehave shown that phosphorylation of this residue is not essential for checkpoint controls to prevent mitosis. We have investigated the basis for checkpoint controls in this organism and show that these controls can prevent entry into mitosis even in cells which have fully activated the cyclin B (Clb)-associated forms of the budding yeast homolog of p34cdc2, p34CDC28, as assayed by histone H1 kinase activity. However, the active complexes in checkpoint-arrested cells are smaller than those in cycling cells, suggesting that assembly of mitosis-inducing complexes requires additional steps following histone H1 kinase activation.