Condensin and the spindle midzone prevent cytokinesis failure induced by chromatin bridges in C. elegans embryos.
Condensin and the spindle midzone prevent cytokinesis failure induced by chromatin bridges in C. elegans embryos.
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DOI：
10.1016/j.cub.2013.04.028
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发表时间：
2013-06-03
期刊：
影响因子：
9.2
通讯作者：
Chan, Raymond C.
中科院分区：
文献类型：
--
作者：
Bembenek, Joshua N.;Verbrugghe, Koen J. C.;Khanikar, Jayshree;Csankovszki, Gyoergyi;Chan, Raymond C.
在细胞分裂期间，染色体必须在胞质分裂开始之前清除卵裂沟的路径。哺乳动物细胞中的裂解检查点在存在染色质障碍物的情况下稳定切割沟。这提供了在卵裂沟退化或断裂染色体之前解决障碍的时间，从而防止非整倍体或DNA损伤。在所提出的脱落检查点的机制途径中，有两个未回答的问题涉及以下因素：1）解决阻塞，和2）协调阻塞解决与胞质分裂延迟。我们发现1细胞和2细胞C.线虫胚胎在基本的染色体分离因子：拓扑异构酶IITOP-2、CENP-AHCP-3、粘着蛋白和在较小程度上的凝聚蛋白耗尽后抑制沟退化。染色质障碍激活了纺锤体中间区的Aurora BAIR-2，这是其他系统中的解离检查点所需要的。凝聚素I（而不是凝聚素II）定位于后期纺锤体中区和正常胞质分裂期间的中体。有趣的是，浓缩蛋白I是丰富的染色质桥和附近的中间区/midbody在AIR-2依赖的方式。AIR-2、纺锤体中间区或凝聚素的破坏以染色质阻塞依赖的方式导致胞质分裂失败。对缺乏凝聚素的胚胎的检查发现了染色质障碍物的分辨率和稳定卵裂沟的维持方面的缺陷。我们推测，凝聚素I被极光BAIR-2招募，以帮助解决染色质阻塞，也有助于产生信号，以维持胞质分裂的延迟。
During cell division, chromosomes must clear the path of the cleavage furrow before the onset of cytokinesis. The abscission checkpoint in mammalian cells stabilizes the cleavage furrow in the presence of a chromatin obstruction. This provides time to resolve the obstruction before the cleavage furrow regresses or breaks the chromosomes, preventing aneuploidy or DNA damage. Two unanswered questions in the proposed mechanistic pathway of the abscission checkpoint concern factors involved in 1) resolving the obstructions, and 2) coordinating obstruction resolution with the delay in cytokinesis. We found that the 1-cell and 2-cell C. elegans embryos suppress furrow regression following depletion of essential chromosome segregation factors: topoisomerase IITOP-2, CENP-AHCP-3, cohesin, and to a lesser degree, condensin. Chromatin obstructions activated Aurora BAIR-2 at the spindle midzone, which is needed for the abscission checkpoint in other systems. Condensin I, but not condensin II, localizes to the spindle midzone in anaphase and to the midbody during normal cytokinesis. Interestingly, condensin I is enriched on chromatin bridges and near the midzone/midbody in an AIR-2 dependent manner. Disruption of AIR-2, the spindle midzone or condensin leads to cytokinesis failure in a chromatin-obstruction-dependent manner. Examination of the condensin-deficient embryos uncovered defects in both the resolution of the chromatin obstructions and the maintenance of the stable cleavage furrow. We postulate that condensin I is recruited by Aurora BAIR-2 to aid in the resolution of chromatin obstructions and also helps generate a signal to maintain the delay in cytokinesis.
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