Ribeiro Susana A, Gatlin Jesse C, Dong Yimin, Joglekar Ajit, Cameron Lisa, Hudson Damien F, Farr Christine J, McEwen Bruce F, Salmon Edward D, Earnshaw William C, Vagnarelli Paola
Wellcome Trust Centre for Cell Biology, Institute of Cell and Molecular Biology, University of Edinburgh, Edinburgh EH9 3JR, United Kingdom.
Mol Biol Cell. 2009 May;20(9):2371-80. doi: 10.1091/mbc.e08-11-1127. Epub 2009 Mar 4.
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.
当染色体在中期排列并双定向时,着丝粒染色质的弹性拉伸会对抗有丝分裂纺锤体施加在姐妹动粒上的拉力。我们在此表明,凝聚素ATP酶活性是着丝粒硬度和功能的重要调节因子。当对着丝粒施加拉力时,凝聚素缺失会使着丝粒染色质的硬度降低50%。然而,凝聚素对于着丝粒正常水平的压缩(静止长度)并非必需,这可能取决于控制高阶染色质折叠的其他因素。动粒的结构或运动性也不需要凝聚素。凝聚素缺失导致的硬度丧失会产生异常的、不协调的姐妹动粒运动,导致中期板附近Mad2(+)动粒增加,并延迟后期开始。