Exercise-dependent formation of new junctions that promote STIM1-Orai1 assembly in skeletal muscle.

ABSTRACT: Store-operated Ca²⁺ entry (SOCE), a ubiquitous mechanism that allows recovery of Ca²⁺ ions from the extracellular space, has been proposed to limit fatigue during repetitive skeletal muscle activity. However, the subcellular location for SOCE in muscle fibers has not been unequivocally identified. Here we show that exercise drives a significant remodeling of the sarcotubular system to form previously unidentified junctions between the sarcoplasmic reticulum (SR) and transverse-tubules (TTs). We also demonstrate that these new SR-TT junctions contain the molecular machinery that mediate SOCE: stromal interaction molecule-1 (STIM1), which functions as the SR Ca²⁺ sensor, and Orai1, the Ca²⁺-permeable channel in the TT. In addition, EDL muscles isol

SUBMITTER: Boncompagni S 

PROVIDER: S-EPMC5660245 | biostudies-literature | 2017 Oct

REPOSITORIES: biostudies-literature