Defects in Saccharomyces cerevisiae protein phosphatase type I activate the spindle/kinetochore checkpoint
Defects in Saccharomyces cerevisiae protein phosphatase type I activate the spindle/kinetochore checkpoint
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DOI：
10.1101/gad.13.5.517
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发表时间：
1999-03-01
影响因子：
10.5
通讯作者：
Tatchell, K
中科院分区：
文献类型：
--
作者：
Bloecher, A;Tatchell, K
酿酒酵母中1型蛋白磷酸酶（glc7-129）的条件等位基因导致G(2)/M细胞的第一周期阻滞，其特征是细胞具有短纺锤体和高H1激酶活性。执行点实验表明，在有丝分裂后期完成之前，Glc7p在G(2)/M细胞中发挥作用。glc7-129细胞中纺锤体/着丝点检查点的缺失消除了G(2)/M细胞周期阻滞，并伴随染色体丢失的增加和生存能力的降低。这些结果支持Glc7p在调节纺锤体附着到纺锤体上的作用，这是一个由纺锤体/着丝点检查点监测的事件。
A conditional allele of type 1 protein phosphatase (glc7-129) in Saccharomyces cerevisiae causes first cycle arrest in G(2)/M, characterized by cells with a short spindle and high H1 kinase activity. Point-of-execution experiments indicate Glc7p function is required in G(2)/M lust before anaphase for the completion of mitosis. Loss of the spindle/kinetochore checkpoint in glc7-129 cells abolishes the G(2)/M cell cycle arrest with a concomitant increase in chromosome loss and reduced viability. These results support a role for Glc7p in regulating kinetochore attachment to the spindle, an event monitored by the spindle/kinetochore checkpoint.