Nonmuscle myosin II is a critical regulator of clathrin-mediated endocytosis

Traffic. 2014 Apr;15(4):418-32. doi: 10.1111/tra.12152. Epub 2014 Feb 12.


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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / metabolism
  • Animals
  • Clathrin / physiology*
  • Endocytosis / physiology*
  • Mice
  • Mice, Knockout
  • Muscles / physiology
  • Myosin Type II / genetics
  • Myosin Type II / physiology*
  • Transferrin / metabolism


  • Actins
  • Clathrin
  • Transferrin
  • Myosin Type II