Frustration of endocytosis potentiates compression-induced receptor signaling

Francesco Baschieri, Dahiana Le Devedec, Samuel Tettarasar, Nadia Elkhatib, Guillaume Montagnac

    Résultats de recherche: Contribution à un journalArticleRevue par des pairs

    9 Citations (Scopus)

    Résumé

    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 frustration of CCSs and that CCSs are required to potentiate receptor-mediated signaling in these conditions. We show that cell compression stalled CCS dynamics and slowed down the dynamic exchange of CCS components. As previously reported, compression-induced paracrine activation of the epidermal growth factor receptor (EGFR) was the primary cause of ERK (ERK1 and ERK2, also known as MAPK3 and MAPK1, respectively) activation in these conditions. We observed that 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 for the adaptation of the cell to its environment.

    langue originaleAnglais
    Numéro d'articlejcs239681
    journalJournal of Cell Science
    Volume133
    Numéro de publication17
    Les DOIs
    étatPublié - 1 sept. 2021

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