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

被引:233
作者
Norden, C
Mendoza, M
Dobbelaere, J
Kotwaliwale, CV
Biggins, S
Barral, Y [1 ]
机构
[1] ETH, Inst Biochem, Dept Biol, CH-8093 Zurich, Switzerland
[2] Fred Hutchinson Canc Res Ctr, Div Basic Sci, Seattle, WA 98109 USA
基金
美国国家卫生研究院;
关键词
D O I
10.1016/j.cell.2006.01.045
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:85 / 98
页数:14
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