Cross-talk between the calcium channel TRPV4 and reactive oxygen species interlocks adhesive and degradative functions of invadosomes

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• dc.contributor.author Vellino, Sanela
• dc.contributor.author Oddou, Christiane
• dc.contributor.author Rivier, Paul
• dc.contributor.author Boyault, Cyril
• dc.contributor.author Hiriart-Bryant, Edwige
• dc.contributor.author Kraut, Alexandra
• dc.contributor.author Martin, René
• dc.contributor.author Coute, Yohann
• dc.contributor.author Knölker, Hans-Joachim
• dc.contributor.author Valverde, M. A. (Miguel Ángel), 1963-
• dc.contributor.author Albiges-Rizo, Corinne
• dc.contributor.author Destaing, Olivier
• dc.date.accessioned 2022-03-17T10:05:30Z
• dc.date.available 2022-03-17T10:05:30Z
• dc.date.issued 2021
• dc.description.abstract Invadosomes support cell invasion by coupling both acto-adhesive and extracellular matrix degradative functions, which are apparently antagonistic. β1-integrin dynamics regulate this coupling, but the actual sensing mechanism and effectors involved have not yet been elucidated. Using genetic and reverse genetic approaches combined with biochemical and imaging techniques, we now show that the calcium channel TRPV4 colocalizes with β1-integrins at the invadosome periphery and regulates its activation and the coupling of acto-adhesive and degradative functions. TRPV4-mediated regulation of podosome function depends on its ability to sense reactive oxygen species (ROS) in invadosomes' microenvironment and involves activation of the ROS/calcium-sensitive kinase Ask1 and binding of the motor MYO1C. Furthermore, disease-associated TRPV4 gain-of-function mutations that modulate ECM degradation are also implicated in the ROS response, which provides new perspectives in our understanding of the pathophysiology of TRPV4 channelopathies.
• dc.description.sponsorship This work was funded by the Agence Nationale de la Recherche (ANR; invadocontrol; ANR-13-JSV2-0003-01) program and Ligue Contre le Cancer as “Equipe labellisée Ligue 2014” (EL2014.LNCC/CAR), the Spanish Ministry of Economy, Industry, and Competitiveness through grant RTI2018-099718, the institutional “Maria de Maeztu” Program for Units of Excellence in Research and Development, and FEDER funds. S. Vellino was funded by the European Marie-Sklodowska-Curie funding program. Proteomic experiments were partly supported by the Proteomics French Infrastructure (grant ANR-10-INBS-08-01) and Labex GRAL (grant ANR-10-LABX-49-01)
• dc.format.mimetype application/pdf
• dc.identifier.citation Vellino S, Oddou C, Rivier P, Boyaut C, Hirian-Bryant E,Kraut A et al. Cross-talk between the calcium channel TRPV4 and reactive oxygen species interlocks adhesive and degradative functions of invadosomes. J Cell Biol. 2021 Feb 1;220(2):e201910079. DOI: 10.1083/jcb.201910079
• dc.identifier.doi http://dx.doi.org/10.1083/jcb.201910079
• dc.identifier.issn 1540-8140
• dc.identifier.uri http://hdl.handle.net/10230/52709
• dc.language.iso eng
• dc.publisher Rockefeller University Press
• dc.rights © 2021 Vellino et al. This article is distributed under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/)
• dc.rights.accessRights info:eu-repo/semantics/openAccess
• dc.rights.uri https://creativecommons.org/licenses/by-nc-sa/4.0/
• dc.subject.other Genètica
• dc.title Cross-talk between the calcium channel TRPV4 and reactive oxygen species interlocks adhesive and degradative functions of invadosomes
• dc.type info:eu-repo/semantics/article
• dc.type.version info:eu-repo/semantics/publishedVersion