CLIC-dependent internalization of caveolin-1 to lysosomal vacuoles in response to osmotic regulation
Abstract
Originally thought to be a major endocytic portal, caveolae function as a membrane buffer, whereby caveolae flattening protects the plasma membrane from rupture under mechanical stress, such as hypotonic shock. However, the fate of the caveolae coat protein caveolin-1 upon caveolae flattening is not known. Here, extended hypotonic shock induces ubiquitin-independent, CLIC-dependent endocytosis of caveolin-1 to large, intracellular, CD44-positive, pH-neutral lysosomal vacuoles negative for multivesicular body markers. Caveolin-1 recycles from these vacuoles to the plasma membrane upon return to isotonic conditions. Caveolin-1 internalization occurs upon reduced cell volume due to extended hypotonic shock as well as in low-tension cells grown on reduced-stiffness hydrogels. Upon hypertonic shock, caveolin-1 internalization occurs in PC3 cells, lacking cavin-1 and caveolae, and is inhibited upon cavin-1 reintroduction. CLIC endocytosis of non-caveolar caveolin-1 to neutral pH lysosomal vacuoles identifies a non-caveolar endocytic and recycling pathway for caveolin-1 in response to reduced membrane tension.
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BibTeX
@article{wong2026clicdependent,
title = {{CLIC-dependent internalization of caveolin-1 to lysosomal vacuoles in response to osmotic regulation}},
author = {Timothy Wong and Matheus Lima and Aditya Nagrath and Y. Lydia Li and Bharat Joshi and Fuiboon Kai and Ivan Robert Nabi},
journal = {Cell Reports},
year = {2026},
month = oct,
doi = {10.1016/j.celrep.2026.117373},
url = {https://hal.science/hal-05785144v1},
note = {CC BY-NC},
}
RIS
TY - JOUR
TI - CLIC-dependent internalization of caveolin-1 to lysosomal vacuoles in response to osmotic regulation
AU - Timothy Wong
AU - Matheus Lima
AU - Aditya Nagrath
AU - Y. Lydia Li
AU - Bharat Joshi
AU - Fuiboon Kai
AU - Ivan Robert Nabi
PY - 2026
DA - 2026/10/08
JO - Cell Reports
DO - 10.1016/j.celrep.2026.117373
UR - https://hal.science/hal-05785144v1
AB - Originally thought to be a major endocytic portal, caveolae function as a membrane buffer, whereby caveolae flattening protects the plasma membrane from rupture under mechanical stress, such as hypotonic shock. However, the fate of the caveolae coat protein caveolin-1 upon caveolae flattening is not known. Here, extended hypotonic shock induces ubiquitin-independent, CLIC-dependent endocytosis of caveolin-1 to large, intracellular, CD44-positive, pH-neutral lysosomal vacuoles negative for multivesicular body markers. Caveolin-1 recycles from these vacuoles to the plasma membrane upon return to isotonic conditions. Caveolin-1 internalization occurs upon reduced cell volume due to extended hypotonic shock as well as in low-tension cells grown on reduced-stiffness hydrogels. Upon hypertonic shock, caveolin-1 internalization occurs in PC3 cells, lacking cavin-1 and caveolae, and is inhibited upon cavin-1 reintroduction. CLIC endocytosis of non-caveolar caveolin-1 to neutral pH lysosomal vacuoles identifies a non-caveolar endocytic and recycling pathway for caveolin-1 in response to reduced membrane tension.
SN - 2211-1247
SN - 2211-1247
ER -