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Nonmuscle Myosin II Is a Critical Regulator of Clathrin‐Mediated Endocytosis |
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| Authors: | Indra Chandrasekar Zoe M Goeckeler Stephen G Turney Peter Wang Robert B Wysolmerski Robert S Adelstein Paul C Bridgman |
| Institution: | 1. Department of Anatomy and Neurobiology, Washington University School of Medicine, , St. Louis, MO, 63110 USA;2. Present address: Sanford Children's Health Research Center, Sanford Research, Sioux Falls, SD 57104, USA;3. Department of Neurobiology and Anatomy, Mary Babb Randolph Cancer Center, West Virginia University School of Medicine, , Morgantown, WV, 26506 USA;4. Department of Molecular and Cellular Biology, Harvard University, , Cambridge, MA, 02138 USA;5. Laboratory of Molecular Cardiology, NHLBI, NIH, , Bethesda, MD, 20892 USA |
| Abstract: | Variable requirements for actin during clathrin‐mediated endocytosis (CME) may be related to regional or cellular differences in membrane tension. To compensate, local regulation of force generation may be needed to facilitate membrane curving and vesicle budding. Force generation is assumed to occur primarily through actin polymerization. Here we examine the role of myosin II using loss of function experiments. Our results indicate that myosin II acts on cortical actin scaffolds primarily in the plane of the plasma membrane (bottom arrow) to generate changes that are critical for enhancing CME progression.  |
| Keywords: | actin clathrin endocytosis myosin II |