Condensin Regulates the Stiffness of Vertebrate Centromeres

Molecular Biology of the Cell - Tập 20 Số 9 - Trang 2371-2380 - 2009
Susana A. Ribeiro1, Jesse C. Gatlin2, Yimin Dong3, Ajit P. Joglekar2, Lisa Cameron2, Damien F. Hudson1,4, Christine J. Farr5, Bruce F. McEwen3, Edward D. Salmon2, William C. Earnshaw1, Paola Vagnarelli1
1*Wellcome Trust Centre for Cell Biology, Institute of Cell and Molecular Biology, University of Edinburgh, Edinburgh EH9 3JR, United Kingdom;
2Department of Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599;
3Wadsworth Center, New York State Department of Health, Albany, NY 12201
4Chromosome and Chromatin Research, Murdoch Children's Research Institute, Royal Children's Hospital, Melbourne 3052, Australia; and
5Department of Genetics, University of Cambridge, Cambridge, CB2 3EH, United Kingdom

Tóm tắt

When chromosomes are aligned and bioriented at metaphase, the elastic stretch of centromeric chromatin opposes pulling forces exerted on sister kinetochores by the mitotic spindle. Here we show that condensin ATPase activity is an important regulator of centromere stiffness and function. Condensin depletion decreases the stiffness of centromeric chromatin by 50% when pulling forces are applied to kinetochores. However, condensin is dispensable for the normal level of compaction (rest length) of centromeres, which probably depends on other factors that control higher-order chromatin folding. Kinetochores also do not require condensin for their structure or motility. Loss of stiffness caused by condensin-depletion produces abnormal uncoordinated sister kinetochore movements, leads to an increase in Mad2(+) kinetochores near the metaphase plate and delays anaphase onset.

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Thông tin xuất bản

Molecular Biology of the Cell

Tập 20 Số 9

2371-2380

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