Structural alterations of the mitotic apparatus induced by the heat shock response in Drosophila cells
Structural alterations of the mitotic apparatus induced by the heat shock response in Drosophila cells
复制标题
DOI：
10.1016/s0248-4900(99)80082-3
复制
发表时间：
1997-03-01
影响因子：
2.7
通讯作者：
Marcaillou, C
中科院分区：
文献类型：
--
作者：
Debec, A;Marcaillou, C
在超微结构水平上研究了果蝇培养细胞有丝分裂器的一般构筑。它的两个主要特征是一个非常极化的纺锤体和一个强烈的区隔，这是由核膜的大量残留物确保的。在早期胚胎的快速合体分裂中，已经有过这种区划的报道；在这些周期较长的细胞中也有类似的发现，有力地表明这种组织构成了果蝇有丝分裂的一般机制。我们观察了37℃热休克20、50或120分钟后这些结构的改变。与间期细胞相反，有丝分裂细胞对高温非常敏感。这种胁迫处理导致有丝分裂纺锤体的破坏，高尔基体的重现和延伸，微管成核的失活和中心体的解体。这个细胞器似乎是第一个受到热休克反应影响的细胞器。中心体不仅失活，而且在结构上也受到影响。在热应激后的恢复期，有丝分裂细胞在中心粒周围表现出明显的电子致密物质的环状堆积。我们得出结论，在果蝇细胞中，有丝分裂阶段，更具体地说，中心体，是应激反应的目标。
The general architecture of the mitotic apparatus was studied at the ultrastructural level in Drosophila cultured cells. Its two main characteristics are a very polarized spindle and a strong compartmentalization, ensured by large remnants of the nuclear envelope. Such compartmentalization has previously been reported for the rapid syncytial divisions of the early embryo; a similar finding in these cells with a long cycle strongly suggests that this organization constitutes a general mechanism for mitosis in Drosophila. We followed the modifications of these structures after a heat shock of 20, 50 or 120 min at 37 degrees C. Contrary to interphase cells, mitotic cells appear very sensitive to hyperthermia. This stress treatment induced a disruption of the mitotic spindle, a reappearance and an extension of the Golgi apparatus, an inactivation of microtubule nucleation and a disorganization of the centrosome. This organelle seems the first to be affected by the heat shock response. The centrosome is not only inactivated, but also is structurally affected. During the recovery phase after heat stress, the mitotic cells presented a remarkable ring-shaped accumulation of electron-dense material around the centrioles. We conclude that in Drosophila cells the mitotic phase, and more specifically the centrosome, are targets of the stress response.