The CaV1.1 protein senses the electrical activity of the plasma membrane for the processes of excitation-contraction coupling (ECC) and excitation-transcription coupling (ETC) of skeletal muscle cells. For ECC, CaV1.1 controls the activity of the type 1 ryanodine receptor (RyR1) Ca2+ release channel in the reticulum membrane. For ETC, CaV1.1 controls the activity of pannexin 1 (Panx1), a plasma membrane ATP channel responsible for ATP exit and consequent activation of a signaling pathway involved in muscle plasticity. The present project aimed at -determining the potential role of Panx1 as a partner in ECC, -characterizing Panx1 functional properties in single isolated muscle fibers, investigating the function of ECC in a disease model suspected to be associated with Panx1 dysfunction. Down-expression of Panx1 in muscle fibers is associated with altered functions of CaV1.1 and RyR1 during ECC. Furthermore, Panx1 pharmacological blockers also alter Ca2+ signaling in muscle fibers. Overall results establish a role for Panx1 in the control of muscle Ca2+ homeostasis and ECC. We attempted to detect Panx1-mediated ATP release at the single muscle fiber level using biological sensors: either ATP-dependent K+ channels or ionotropic purinergic receptors. Both methods work but did not allow detection of Panx1-induced ATP release in a reliable manner. Altered Panx1 function is suspected in muscles under type 2 diabetes conditions. We tested whether ECC is altered in that situation and contributes to the associated muscle weakness. We found that it is not the case. ECC is remarkably preserved in muscle fibers from a diet-induced mouse model of diabetes and obesity. ; La protéine membranaire Cav1.1 détecte l’activité électrique de la membrane plasmique pour le couplage excitation-contraction (CEC) et excitation-transcription (CET) des cellules musculaires. Pour le CET, CaV1.1 contrôle le canal calcique RyR1 dans la membrane du réticulum. Pour le CET, CaV1.1 contrôle la pannexine 1 (Panx1), un canal à ATP de la membrane ...
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