MYOSIN IS INVOLVED IN POSTMITOTIC CELL SPREADING

被引:274
作者
CRAMER, LP
MITCHISON, TJ
机构
[1] Dept. of Cell. and Molec. Pharmacol., University of California, San Francisco
[2] Dept. of Cell. and Molec. Pharmacol., University of California, San Francisco, CA 94143-0450
关键词
D O I
10.1083/jcb.131.1.179
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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 deter mined 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.
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页码:179 / 189
页数:11
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