Myosin is involved in postmitotic cell spreading.
Myosin is involved in postmitotic cell spreading.
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DOI：
10.1083/jcb.131.1.179
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发表时间：
1995-10
期刊：
影响因子：
--
通讯作者：
Mitchison TJ
中科院分区：
文献类型：
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作者：
Cramer LP;Mitchison TJ
我们通过抑制剂研究、延时视频显微镜和免疫荧光研究了肌球蛋白在有丝分裂后三指肾 (PtK2) 细胞扩散中的作用。我们还确定了有丝分裂后扩散细胞中肌动蛋白丝的空间组织和极性。我们发现丁二酮单肟 (BDM) 是一种已知的肌肉肌球蛋白 II 抑制剂，可抑制非肌肉肌球蛋白 II 和肌球蛋白 V 腺苷三磷酸酶。 BDM 可逆地抑制 PtK2 有丝分裂后细胞扩散。李斯特菌的运动不受该药物的影响。电子显微镜研究表明，展开边缘中的一些肌动蛋白丝是肌动蛋白束的一部分，这些肌动蛋白束也存在于连接到展开边缘和基底（回缩纤维）的长而细的结构中，并且该肌动蛋白的 90% 在展开方向上具有倒刺末端。扩展边缘中剩余的肌动蛋白具有更加随机的方向和空间排列。肌球蛋白 II 与伸展细胞边缘的肌动蛋白聚合物相关，但与回缩纤维无关。肌球蛋白 II 被排除在铺展结束时从细胞边缘突出的片状伪足之外。我们认为传播涉及肌球蛋白，可能是肌球蛋白 II。
We have investigated a role for myosin in postmitotic Potoroo tridactylis kidney (PtK2) cell spreading by inhibitor studies, time- lapse video microscopy, and immunofluorescence. We have also determined the spatial organization and polarity of actin filaments in postmitotic spreading cells. We show that butanedione monoxime (BDM), a known inhibitor of muscle myosin II, inhibits nonmuscle myosin II and myosin V adenosine triphosphatases. BDM reversibly inhibits PtK2 postmitotic cell spreading. Listeria motility is not affected by this drug. Electron microscopy studies show that some actin filaments in spreading edges are part of actin bundles that are also found in long, thin, structures that are connected to spreading edges and substrate (retraction fibers), and that 90% of this actin is oriented with barbed ends in the direction of spreading. The remaining actin in spreading edges has a more random orientation and spatial arrangement. Myosin II is associated with actin polymer in spreading cell edges, but not retraction fibers. Myosin II is excluded from lamellipodia that protrude from the cell edge at the end of spreading. We suggest that spreading involves myosin, possibly myosin II.