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Vol. 20, Issue 9, 2371-2380, May 1, 2009

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Condensin Regulates the Stiffness of Vertebrate Centromeres

Susana A. Ribeiro^*, Jesse C. Gatlin, Yimin Dong, Ajit Joglekar, Lisa Cameron, Damien F. Hudson^*,, Christine J. Farr^||, Bruce F. McEwen, Edward D. Salmon, William C. Earnshaw^*, and Paola Vagnarelli^*

*Wellcome Trust Centre for Cell Biology, Institute of Cell and Molecular Biology, University of Edinburgh, Edinburgh EH9 3JR, United Kingdom; Department of Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599; Wadsworth Center, New York State Department of Health, Albany, NY 12201; Chromosome and Chromatin Research, Murdoch Children's Research Institute, Royal Children's Hospital, Melbourne 3052, Australia; and ^||Department of Genetics, University of Cambridge, Cambridge CB2 3EH, United Kingdom

Submitted November 17, 2008; Revised February 20, 2009; Accepted February 24, 2009
Monitoring Editor: Stephen Doxsey

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.

Address correspondence to: William C. Earnshaw (bill.earnshaw{at}ed.ac.uk) or Paola Vagnarelli (p.vagnarelli{at}ed.ac.uk).

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