Beaudouin Joël, Gerlich Daniel, Daigle Nathalie, Eils Roland, Ellenberg Jan
Gene Expression and Cell Biology/Biophysics Programmes, European Molecular Biology Laboratory, D-69117. Heidelberg, Germany
Cell. 2002 Jan 11;108(1):83-96. doi: 10.1016/s0092-8674(01)00627-4.
The mechanism of nuclear envelope breakdown (NEBD) was investigated in live cells. Early spindle microtubules caused folds and invaginations in the NE up to one hour prior to NEBD, creating mechanical tension in the nuclear lamina. The first gap in the NE appeared before lamin B depolymerization, at the site of maximal tension, by a tearing mechanism. Gap formation relaxed this tension and dramatically accelerated the rate of chromosome condensation. The hole produced in the NE then rapidly expanded over the nuclear surface. NE fragments remaining on chromosomes were removed toward the centrosomes in a microtubule-dependent manner, suggesting a mechanism mediated by a minus-end-directed motor.
在活细胞中研究了核膜破裂(NEBD)的机制。在NEBD前一小时,早期纺锤体微管在核膜上引起褶皱和内陷,在核纤层中产生机械张力。NE的第一个缺口出现在核纤层B解聚之前,在最大张力部位,通过撕裂机制形成。缺口的形成缓解了这种张力,并显著加速了染色体凝聚的速度。然后在NE中产生的孔迅速在核表面扩展。留在染色体上的NE片段以微管依赖的方式向中心体移动,提示这是一种由负端定向马达介导的机制。