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Article | Mechanotransduction by Membrane Proteins
Jonathan R.M. Millet, Luis O. Romero, Jungsoo Lee, Briar Bell, Valeria Vásquez
Millet et al. show that the C. elegans orthologue of the PIEZO family, PEZO-1, is a mechanosensitive ion channel involved in food sensation and in regulating pharyngeal function in the nematode.
Zhuyuan Chen, Sheng Lin, Tianze Xie, Jin-Ming Lin, Cecilia M. Canessa
Chen et al. computationally model the open conformation of the hASIC1a channel to predict that mutations that eliminate channel selectivity cause a widening of the GAS belt. Their findings implicate the GAS belt diameter in channel kinetics and ion selectivity.
Hind Albadrani, T. Ammar, Michael Bader, Jean-Marc Renaud
Albadrani et al. studied the potential of angiotensin 1–7 to prevent the atrophy that normally ensues muscle denervation. Increasing angiotensin 1–7 levels do not prevent muscle mass loss in denervated muscles but maintain normalized tetanic force to cross-sectional area and membrane excitability for up to 28 d.
Catherine E. Morris, Joshua J. Wheeler, Béla Joos
Morris et al. use a computational model of Pump-Leak/Donnan ion homeostasis to suggest that the Donnan dominated steady-state of skeletal muscle fibers underpins their longevity in the face of the structural and metabolic injuries incurred with Duchenne muscular dystrophy.
Marina Angelini, Arash Pezhouman, Nicoletta Savalli, Marvin G. Chang, Federica Steccanella, Kyle Scranton, Guillaume Calmettes, Michela Ottolia, Antonios Pantazis, Hrayr S. Karagueuzian, James N. Weiss, Riccardo Olcese
Angelini et al. show that reducing late L-type Ca2+ current with the purine analogue roscovitine is sufficient to suppress ventricular arrhythmias in myocytes and ex vivo hearts. By preserving the early component of ICa,L, this strategy is expected to largely maintain contractility, an advantage over Ca2+ channel blockers.
Angélique Desplat, Virginie Penalba, Emeline Gros, Thibaud Parpaite, Bertrand Coste, Patrick Delmas
Desplat et al. show that the Piezo1 channel mediates Ca2+ entry into mouse cholangiocytes as a result of mechanical stress due to cell swelling. Piezo1 thus activates and forms complexes with Pannexin1, which result in force-induced ATP release and signal amplification through P2X4R.
Article | Excitation–Contraction Coupling
Francisco Jaque-Fernández, Gonzalo Jorquera, Jennifer Troc-Gajardo, France Pietri-Rouxel, Christel Gentil, Sonja Buvinic, Bruno Allard, Enrique Jaimovich, Vincent Jacquemond, Mariana Casas
Jaque-Fernández et al. show that downregulation of CaV1.1 in muscle fibers elevates ATP release, whereas downregulation of Panx1 depresses depolarization-induced intracellular Ca2+ release. They conclude that Panx1 is a reciprocal partner of CaV1.1 for both excitation–contraction and excitation–transcription coupling.

Related Articles from Rockefeller University Press

Issue Cover
Current Issue
Volume 153,
Issue 11,
November 1, 2021
Reviews & Opinions
Research News
Ben Short
JGP study shows that a mechanosensitive complex containing Piezo1 and Pannexin1 couples osmotic pressure to ATP secretion in bile duct cholangiocytes.
Luis A. Gonano, Alicia Mattiazzi
This commentary is on the paper by Angelini et al. Here, we set the original paper in the context of triggered arrhythmias, particularly early after depolarizations (EADs), emphasizing the importance of pharmacologically inhibiting late Ca2+ current to prevent EADs without affecting myocardial contractility.
Massimo Reconditi, Elisabetta Brunello, Luca Fusi, Marco Linari, Vincenzo Lombardi, Malcolm Irving, Gabriella Piazzesi
Activation of skeletal muscle involves unfolding of myosin motors from their OFF conformation in resting muscle. X-ray diffraction from muscles contracting at longer sarcomere length show that motor unfolding does not depend on the availability of local actin-binding sites.

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