Mammalian spindle orientation and position respond to changes in cell shape in a dynein-dependent fashion
Mammalian spindle orientation and position respond to changes in cell shape in a dynein-dependent fashion
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DOI：
10.1091/mbc.11.5.1765
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发表时间：
2000-05-01
影响因子：
3.3
通讯作者：
Wang, YL
中科院分区：
文献类型：
--
作者：
O'Connell, CB;Wang, YL
在动物细胞中，有丝分裂纺锤体的定位对于确定细胞分裂的平面和子细胞的大小比例至关重要。我们利用显微镜、显微操作和显微注射在大鼠上皮细胞系中描述了这种现象。未经处理的细胞将有丝分裂纺锤体定位在其几何中心附近，纺锤体轴线大致平行于细胞的长轴。最初方向错误的纺锤体经过了定向。并引起了后期发病的延迟。为了进一步了解这一过程，我们用一根钝化的玻璃针轻轻变形细胞，以改变皮层和纺锤体之间的空间关系。这种操作在中期和/或中期诱导纺锤体运动或旋转；后期，直到主轴达到相对于变形形状的适当位置。低剂量诺可达唑或微量注射抗动力蛋白抗体均可抑制纺锤体定位，这显然是由于动力蛋白和/或星状微管的组织被破坏。我们的研究结果表明，有丝分裂细胞持续监测和维持纺锤体相对于皮层的位置。这一过程可能是由星状微管、运动蛋白动力蛋白和细胞皮层之间的相互作用驱动的，并可能构成有丝分裂检查点机制的一部分。
In animal cells, positioning of the mitotic spindle is crucial for defining the plane of cytokinesis and the size ratio of daughter cells. We have characterized this phenomenon in a rat epithelial cell line using microscopy, micromanipulation, and microinjection. Unmanipulated cells position the mitotic spindle near their geometric center, with the spindle axis lying roughly parallel to the long axis of the cell. Spindles that were initially misoriented underwent directed. rotation and caused a delay in anaphase onset. To gain further insight into this process, we gently deformed cells with a blunted glass needle to change the spatial relationship between the cortex and spindle. This manipulation induced spindle movement or rotation in metaphase and/or;anaphase, until the spindle reached a proper position relative to the deformed shape. Spindle positioning was inhibited by either treatment with low doses of nocodazole or microinjection of antibodies against dynein, apparently due to the disruption of the organization of dynein and/or astral microtubules. Our results suggest that mitotic cells continuously monitor and maintain the position of the spindle relative to the cortex. This process is Likely driven by interactions among astral microtubules, the motor protein dynein, and the cell cortex and may constitute part of a mitotic checkpoint mechanism.