The NoCut pathway links completion of cytokinesis to spindle midzone funiction to prevent chromosome breakage
The NoCut pathway links completion of cytokinesis to spindle midzone funiction to prevent chromosome breakage
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DOI：
10.1016/j.cell.2006.01.045
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发表时间：
2006-04-07
期刊：
影响因子：
64.5
通讯作者：
Barral, Y
中科院分区：
文献类型：
--
作者：
Norden, C;Mendoza, M;Barral, Y
在后期，纺锤体伸长将姐妹染色单体拉开，直至每一对完全分离。接着，胞质分裂在分离的染色体之间使细胞分裂。是什么确保胞质分裂仅在所有染色体臂都被拉出分裂平面之后才进行，这一点此前并不清楚。在此，我们表明一种我们称之为NoCut的信号通路会延迟纺锤体中区有缺陷的细胞的胞质分裂完成。NoCut依赖于极光激酶Ipl1以及与肌动蛋白结合蛋白相关的Boi1和Boi2，它们以依赖于Ipl1的方式定位于分裂位点，并作为分裂抑制因子发挥作用。NoCut失活会导致胞质分裂机制过早分裂以及染色体断裂，并且在纺锤体伸长有缺陷的细胞中是致命的。我们提出NoCut监测染色质从中区的清除情况，以确保只有在所有染色体都迁移到两极之后胞质分裂才完成。
During anaphase, spindle elongation pulls sister chromatids apart until each pair is fully separated. In turn, cytokinesis cleaves the cell between the separated chromosomes. What ensures that cytokinesis proceeds only after that all chromosome arms are pulled out of the cleavage plane was unknown. Here, we show that a signaling pathway, which we call NoCut, delays the completion of cytokinesis in cells with spindle-midzone defects. NoCut depends on the Aurora kinase Ipl1 and the anillin-related proteins Boi1 and Boi2, which localize to the site of cleavage in an Ipl1-dependent manner and act as abscission inhibitors. Inactivation of NoCut leads to premature abscission and chromosome breakage by the cytokinetic machinery and is lethal in cells with spindle-elongation defects. We propose that NoCut monitors clearance of chromatin from the midzone to ensure that cytokinesis completes only after all chromosomes have migrated to the poles.