Apr 6, 2020

Adaptive actin organization counteracts elevated membrane tension to ensure robust endocytosis

BioRxiv : the Preprint Server for Biology
C. KaplanDavid G. Drubin

Abstract

Clathrin-mediated endocytosis (CME) remains robust despite variations in plasma membrane tension. Actin assembly-mediated force generation becomes essential for CME under high membrane tension, but the underlying mechanisms are not understood. We investigated actin network ultrastructure at each stage of CME by super-resolution imaging. Actin and N-WASP spatial organization indicate that polymerization initiates at the base of clathrin-coated pits and that the actin network then grows away from the plasma membrane. Actin network organization is not tightly coupled to endocytic clathrin coat growth and deformation. Membrane tension-dependent changes in actin organization explain this uncoupling. Under elevated membrane tension, CME dynamics slow down and the actin network grows higher, resulting in greater coverage of the clathrin coat. This adaptive mechanism is especially crucial during the initial membrane curvature-generating stages of CME. Our findings reveal that adaptive force generation by the actin network ensures robust CME progression despite changes in plasma membrane tension.

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Mentioned in this Paper

Genome
Genes
Cell Division
Gene Expression
Intercellular Transport
Cell Cycle
Gene Duplication Abnormality
Species
RNA, Messenger
Phenotype Determination

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