
Endocytosis frustration potentiates compression-induced receptor signalling
Author(s) -
Francesco Baschieri,
Dahiana Le Devedec,
Samuel Tettarasar,
Nadia Elkhatib,
Guillaume Montagnac
Publication year - 2020
Publication title -
journal of cell science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.384
H-Index - 278
eISSN - 1477-9137
pISSN - 0021-9533
DOI - 10.1242/jcs.239681
Subject(s) - paracrine signalling , nanopillar , endocytosis , microbiology and biotechnology , receptor , mapk/erk pathway , biology , signal transduction , autocrine signalling , clathrin , neuroscience , materials science , nanotechnology , genetics , nanostructure
Cells experience mechanical stresses in different physiological and pathological settings. Clathrin-coated structures (CCSs) are sensitive to such perturbations in a way that often results in a mechanical impairment of endocytic budding. Compressive stress is a mechanical perturbation that leads to increased membrane tension and promotes proliferative signals. Here, we report that compression leads to CCSs frustration and that CCSs are required to potentiate receptor-mediated signaling in these conditions. We show that cell compression stalled CCSs dynamics and slowed down the dynamic exchange of CCSs building blocks. As previously reported, compression-induced paracrine activation of the epidermal growth factor receptor (EGFR) was the primary cause of ERK activation in these conditions. We observed that the EGFR was efficiently recruited at CCSs upon compression and that CCSs were required for full ERK activation. In addition, we demonstrated that compression-induced frustrated CCSs could also increase ligand-dependent signaling of other receptors. We thus propose that CCS frustration resulting from mechanical perturbations can potentiate signaling through different receptors with potential important consequences on cell adaptation to its environment.