Spindle multipolarity is prevented by centrosomal clustering

Spindle multipolarity is prevented by centrosomal clustering
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DOI:
10.1126/science.1104905
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发表时间:
2005-01-07
期刊:
影响因子:
56.9
通讯作者:
Saunders, WS
Saunders, WS
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Quintyne, NJ;Reing, JE;Saunders, WS

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大多数肿瘤细胞的特征是基因组不稳定性增加和染色体分离缺陷,通常与中心体的过度扩增和多极纺锤体的形成有关。然而,额外的中心体并不总是导致多极性。在这里,我们描述了阻止非癌细胞中多极纺锤体形成的中心体聚集过程。非癌细胞需要克服这种聚集机制,以允许多极纺锤体以高频率形成。微管运动细胞质动力蛋白是这种凝聚机制的关键部分,在一些肿瘤细胞中,纺锤体蛋白 NuMA 的过度表达会干扰动力蛋白定位,促进多极性。
Most tumor cells are characterized by increased genomic instability and chromosome segregational defects, often associated with hyperamplification of the centrosome and the formation of multipolar spindles. However, extra centrosomes do not always lead to multipolarity. Here, we describe a process of centrosomal clustering that prevented the formation of multipolar spindles in noncancer cells. Noncancer cells needed to overcome this clustering mechanism to allow multipolar spindles to form at a high frequency. The microtubule motor cytoplasmic dynein was a critical part of this coalescing machinery, and in some tumor cells overexpression of the spindle protein NuMA interfered with dynein localization, promoting multipolarity.