As cells migrate and experience forces from their surroundings, they constantly undergo mechanical deformations which reshape their plasma membrane (PM). To maintain homeo-stasis, cells need to detect and restore such changes, not only in terms of overall PM area and tension as previously described, but also in terms of local, nanoscale topography. Here, we describe a novel phenomenon, by which cells sense and restore mechanically induced PM nanoscale defor-mations. We show that cell stretch and subsequent compression reshape the PM in a way that generates local membrane evaginations in the 100 nm scale. These evaginations are recognized by I-BAR proteins, which triggers a burst of actin polymerization mediated by Rac1 and Arp2/3. The actin polymerization burst subsequently re-flattens the evagination, completing the mechanochemical feedback loop. Our results demonstrate a new mechanosensing mechanism for PM shape homeostasis, with potential applicability in different physiological scenarios.

A mechanosensing mechanism controls plasma membrane shape homeostasis at the nanoscale / X. Quiroga, N. Walani, A. Disanza, A. Chavero, A. Mittens, F. Tebar, X. Trepat, R.G. Parton, M.I. Geli, G. Scita, M. Arroyo, A. Le Roux, P. Roca-Cusachs. - In: ELIFE. - ISSN 2050-084X. - 12:(2023 Sep 25), pp. e72316.1-e72316.10. [10.7554/elife.72316]

A mechanosensing mechanism controls plasma membrane shape homeostasis at the nanoscale

G. Scita
Writing – Original Draft Preparation
;
2023

Abstract

As cells migrate and experience forces from their surroundings, they constantly undergo mechanical deformations which reshape their plasma membrane (PM). To maintain homeo-stasis, cells need to detect and restore such changes, not only in terms of overall PM area and tension as previously described, but also in terms of local, nanoscale topography. Here, we describe a novel phenomenon, by which cells sense and restore mechanically induced PM nanoscale defor-mations. We show that cell stretch and subsequent compression reshape the PM in a way that generates local membrane evaginations in the 100 nm scale. These evaginations are recognized by I-BAR proteins, which triggers a burst of actin polymerization mediated by Rac1 and Arp2/3. The actin polymerization burst subsequently re-flattens the evagination, completing the mechanochemical feedback loop. Our results demonstrate a new mechanosensing mechanism for PM shape homeostasis, with potential applicability in different physiological scenarios.
Settore MED/04 - Patologia Generale
   Role of the YAP/TAZ transcriptional regulators in cancer chemoresistance
   MINISTERO DELL'ISTRUZIONE E DEL MERITO
   2017HWTP2K_003
25-set-2023
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/1071688
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