Nonmuscle myosin II is a critical regulator of clathrin-mediated endocytosis.
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.
Department of Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, MO, 63110, USA; Present address: Sanford Children's Health Research Center, Sanford Research, Sioux Falls, SD 57104, USA.
Indra
I
Chandrasekar
Zoe M
ZM
Goeckeler
Stephen G
SG
Turney
Peter
P
Wang
Robert B
RB
Wysolmerski
Robert S
RS
Adelstein
Paul C
PC
Bridgman
D000199:Actins / Q000378:metabolism; D000818:Animals; D002966:Clathrin / Q000502:physiology*; D004705:Endocytosis / Q000502:physiology*; D051379:Mice; D018345:Mice, Knockout; D009132:Muscles / Q000502:physiology; D024462:Myosin Type II / Q000235:genetics / Q000502:physiology*; D014168:Transferrin / Q000378:metabolism
D000199:Actins; D002966:Clathrin; D014168:Transferrin; D024462:Myosin Type II
actin; clathrin; endocytosis; myosin II