Ipl1p-dependent phosphorylation of Mad3p is required for the spindle checkpoint response to lack of tension at kinetochores
Ipl1p-dependent phosphorylation of Mad3p is required for the spindle checkpoint response to lack of tension at kinetochores
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DOI：
10.1101/gad.431507
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发表时间：
2007-05-15
影响因子：
10.5
通讯作者：
Stark, Michael J. R.
中科院分区：
文献类型：
--
作者：
King, Emma M. J.;Rachidi, Najma;Stark, Michael J. R.
纺锤体检查点延迟后期的开始，直到所有染色体都正确附着到微管上。 Ipl1 蛋白激酶 (Aurora B) 需要纠正不适当的着丝粒-微管附着以及对姐妹着丝粒之间缺乏张力的反应。在这里，我们鉴定了检查点蛋白 Mad3p 中被 Ipl1p 磷酸化的残基。当 Mad3p 在两个位点的磷酸化被阻止时，细胞对着丝粒张力降低的反应就会大大减弱。我们的数据为响应姐妹着丝粒张力缺乏的独特检查点途径提供了强有力的证据，其中 Mad3p 的 Ipl1p 依赖性磷酸化是关键步骤。
The spindle checkpoint delays anaphase onset until all chromosomes are correctly attached to microtubules. Ipl1 protein kinase (Aurora B) is required to correct inappropriate kinetochore-microtubule attachments and for the response to lack of tension between sister kinetochores. Here we identify residues in the checkpoint protein Mad3p that are phosphorylated by Ipl1p. When phosphorylation of Mad3p at two sites is prevented, the cell's response to reduced kinetochore tension is dramatically curtailed. Our data provide strong evidence for a distinct checkpoint pathway responding to lack of sister kinetochore tension, in which Ipl1p-dependent phosphorylation of Mad3p is a key step.