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

Indra Chandrasekar, Zoe M. Goeckeler, Stephen G. Turney, Peter Wang, Robert B. Wysolmerski, Robert S. Adelstein, Paul C. Bridgman

Research output: Contribution to journalArticlepeer-review

32 Scopus citations


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.

Original languageEnglish
Pages (from-to)418-432
Number of pages15
Issue number4
StatePublished - Apr 2014


  • Actin
  • Clathrin
  • Endocytosis
  • Myosin II


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