Boettner DR, Friesen H, Andrews B, Lemmon SK

The role of clathrin light chain (CLC) in clathrin-mediated endocytosis is not completely understood. Previous studies have shown that the CLC N-terminus (CLC-NT) binds the Hip1/Hip1R/Sla2 family of membrane/actin binding factors and that overexpression of the CLC-NT in yeast suppresses endocytic defects of clathrin heavy chain mutants. To elucidate the ...

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mechanistic basis for this suppression, we performed Synthetic Genetic Array analysis with a clathrin CLC-NT deletion mutation (clc1-Δ19-76). clc1-Δ19-76 suppressed the internalization defects of null mutations in three late endocytic factors: amphiphysins (rvs161 and rvs167) and verprolin (vrp1). In actin sedimentation assays CLC binding to Sla2 inhibited Sla2 interaction with F-actin. Furthermore, clc1-Δ19-76 suppression of the rvs and vrp phenotypes required the Sla2 actin binding THATCH domain, suggesting that clc1-Δ19-76 promotes internalization by prolonging actin engagement by Sla2. We propose that CLC directs endocytic progression by pruning the Sla2-actin attachments in the clathrin lattice, providing direction for membrane internalization.

Date: Aug. 17, 2011

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