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无切割途径将胞质分裂的完成与纺锤体中间区功能联系起来,以防止染色体断裂。

The NoCut pathway links completion of cytokinesis to spindle midzone function to prevent chromosome breakage.

作者信息

Norden Caren, Mendoza Manuel, Dobbelaere Jeroen, Kotwaliwale Chitra V, Biggins Sue, Barral Yves

机构信息

Institute of Biochemistry, Biology Department, ETH Zurich, 8093 Zurich, Switzerland.

出版信息

Cell. 2006 Apr 7;125(1):85-98. doi: 10.1016/j.cell.2006.01.045.

Abstract

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.

摘要

在后期,纺锤体伸长将姐妹染色单体拉开,直到每对姐妹染色单体完全分离。接着,胞质分裂在分离的染色体之间将细胞切开。此前尚不清楚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。在此,我们表明,我们称之为NoCut的信号通路会延迟有纺锤体中间区缺陷的细胞中胞质分裂的完成。NoCut依赖于极光激酶Ipl1以及与膜收缩环蛋白相关的蛋白质Boi1和Boi2,它们以Ipl1依赖的方式定位于分裂位点并作为分裂抑制因子发挥作用。NoCut的失活会导致胞质分裂机制过早分裂和染色体断裂,并且在有纺锤体伸长缺陷的细胞中是致命的。我们提出,NoCut监测中间区染色质的清除情况,以确保胞质分裂仅在所有染色体都迁移到两极之后才完成。

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