Contributors: Université de Genève = University of Geneva (UNIGE); Max Planck Institute for the Science of Light; Max-Planck-Gesellschaft; Technische Universität Dresden = Dresden University of Technology (TU Dresden); Trafic membranaire et Division cellulaire - Membrane Traffic and Cell Division; Institut Pasteur Paris (IP)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité); Collège Doctoral; Sorbonne Université (SU); Laboratoire de Physique Théorique et Modèles Statistiques (LPTMS); Université Paris-Saclay-Centre National de la Recherche Scientifique (CNRS); Physique et mécanique des milieux hétérogenes (UMR 7636) (PMMH); Ecole Superieure de Physique et de Chimie Industrielles de la Ville de Paris (ESPCI Paris); Université Paris Sciences et Lettres (PSL)-Université Paris Sciences et Lettres (PSL)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité); A.R. acknowledges funding from Human Frontier Science Program Young Investigator Grant RGY0076/2009-C, Swiss National Fund for Research Grants 31003A_149975 and 31003A_173087, Synergia Grant CRSII5_189996, European Research Council Consolidator Grant 311536, and Synergy Grant 951324-R2-TENSION. This work has been supported by Institut Pasteur, CNRS, and ANR (SeptScort) (A.E.). V.A. received a fellowship from the Doctoral School Complexité du Vivant ED515 and La Ligue Contre le Cancer. M.L. was supported by ANR Grant ANR-15-CE13-0004-03 and European Research Council Starting Grant 677532. M.L.’s group belongs to the CNRS consortium Approches Quantitatives du Vivant.; ANR-15-CE13-0004,MuScActin,Approche multi-échelle du couplage mécano-chimique dans la régulation du cytosquelette d'actine(2015); European Project: 311536,EC:FP7:ERC,ERC-2012-StG_20111109,MEMFIS(2013); European Project: 677532,H2020,ERC-2015-STG,MicMactin(2016)
نبذة مختصرة : International audience ; During osmotic changes of their environment, cells actively regulate their volume and plasma membrane tension that can passively change through osmosis. How tension and volume are coupled during osmotic adaptation remains unknown, as their quantitative characterization is lacking. Here, we performed dynamic membrane tension and cell volume measurements during osmotic shocks. During the first few seconds following the shock, cell volume varied to equilibrate osmotic pressures inside and outside the cell, and membrane tension dynamically followed these changes. A theoretical model based on the passive, reversible unfolding of the membrane as it detaches from the actin cortex during volume increase quantitatively describes our data. After the initial response, tension and volume recovered from hypoosmotic shocks but not from hyperosmotic shocks. Using a fluorescent membrane tension probe (fluorescent lipid tension reporter [Flipper-TR]), we investigated the coupling between tension and volume during these asymmetric recoveries. Caveolae depletion and pharmacological inhibition of ion transporters and channels, mTORCs, and the cytoskeleton all affected tension and volume responses. Treatments targeting mTORC2 and specific downstream effectors caused identical changes to both tension and volume responses, their coupling remaining the same. This supports that the coupling of tension and volume responses to osmotic shocks is primarily regulated by mTORC2.
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