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首页> 外文期刊>Journal of cell biology >The Saccharomyces cerevisiae spindle pole body duplication gene MPS1 is part of a mitotic checkpoint.
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The Saccharomyces cerevisiae spindle pole body duplication gene MPS1 is part of a mitotic checkpoint.

机译:酿酒酵母纺锤体极体复制基因MPS1是有丝分裂检查点的一部分。

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摘要

M-phase checkpoints inhibit cell division when mitotic spindle function is perturbed. Here we show that the Saccharomyces cerevisiae MPS1 gene product, an essential protein kinase required for spindle pole body (SPB) duplication (Winey et al., 1991; Lauze et al., 1995), is also required for M-phase check-point function. In cdc31-2 and mps2-1 mutants, conditional failure of SPB duplication results in cell cycle arrest with high p34CDC28 kinase activity that depends on the presence of the wild-type MAD1 checkpoint gene, consistent with checkpoint arrest of mitosis. In contrast, mps1 mutant cells fail to duplicate their SPBs and do not arrest division at 37 degrees C, exhibiting a normal cycle of p34CDC28 kinase activity despite the presence of a monopolar spindle. Double mutant cdc31-2, mps1-1 cells also fail to arrest mitosis at 37 degrees C, despite having SPB structures similar to cdc31-2 single mutants as determined by EM analysis. Arrest of mitosis upon microtubule depolymerization by nocodazole is also conditionally absent in mps1 strains. This is observed in mps1 cells synchronized in S phase with hydroxyurea before exposure to nocodazole, indicating that failure of checkpoint function in mps1 cells is independent of SPB duplication failure. In contrast, hydroxyurea arrest and a number of other cdc mutant arrest phenotypes are unaffected by mps1 alleles. We propose that the essential MPS1 protein kinase functions both in SPB duplication and in a mitotic checkpoint monitoring spindle integrity.
机译:当有丝分裂纺锤体功能受到干扰时,M期检查点会抑制细胞分裂。在这里,我们显示酿酒酵母MPS1基因产物是纺锤极体(SPB)复制所必需的必需蛋白激酶(Winey等,1991; Lauze等,1995),也是M期检查点所必需的。功能。在cdc31-2和mps2-1突变体中,SPB复制的条件性失败会导致细胞周期停滞,并具有高p34CDC28激酶活性,这取决于野生型MAD1检查点基因的存在,与有丝分裂的检查点停止相一致。相比之下,mps1突变细胞无法复制其SPB,并且不会在37摄氏度下停止分裂,尽管存在单极纺锤体,但仍表现出p34CDC28激酶活性的正常循环。双重突变体cdc31-2,mps1-1细胞也无法在37摄氏度下阻止有丝分裂,尽管通过EM分析确定其SPB结构类似于cdc31-2单一突变体。 mps1菌株中也有条件地不存在诺考达唑引起的微管解聚时有丝分裂的停止。这在暴露于诺考达唑之前在S期与羟基脲同步的mps1细胞中观察到,表明mps1细胞中检查点功能的失败与SPB复制失败无关。相反,mps1等位基因不影响羟基脲的阻滞和许多其他的cdc突变阻滞表型。我们建议必需的MPS1蛋白激酶在SPB复制和监测纺锤体完整性的有丝分裂检查点中均起作用。

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