Endophilin-A2-dependent tubular endocytosis promotes plasma membrane repair and parasite invasion.

Abstract:

:Endocytosis of caveolae has previously been implicated in the repair of plasma membrane wounds. Here, we show that caveolin-1-deficient fibroblasts lacking caveolae upregulate a tubular endocytic pathway and have a reduced capacity to reseal after permeabilization with pore-forming toxins compared with wild-type cells. Silencing endophilin-A2 expression inhibited fission of endocytic tubules and further reduced plasma membrane repair in cells lacking caveolin-1, supporting a role for tubular endocytosis as an alternative pathway for the removal of membrane lesions. Endophilin-A2 was visualized in association with cholera toxin B-containing endosomes and was recruited to recently formed intracellular vacuoles containing Trypanosoma cruzi, a parasite that utilizes the plasma membrane wounding repair pathway to invade host cells. Endophilin-A2 deficiency inhibited T. cruzi invasion, and fibroblasts deficient in both caveolin-1 and endophilin-A2 did not survive prolonged exposure to the parasites. These findings reveal a novel crosstalk between caveolin-1 and endophilin-A2 in the regulation of clathrin-independent endocytosis and plasma membrane repair, a process that is subverted by T. cruzi parasites for cell invasion.

journal_name

J Cell Sci

journal_title

Journal of cell science

authors

Corrotte M,Cerasoli M,Maeda FY,Andrews NW

doi

10.1242/jcs.249524

subject

Has Abstract

pub_date

2020-12-01 00:00:00

issue

5

eissn

0021-9533

issn

1477-9137

pii

jcs.249524

journal_volume

134

pub_type

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