Calcium-dependent facilitation and graded deactivation of store-operated calcium entry in fetal skeletal muscle.

Activation of store-operated Ca(2+) entry (SOCE) into the cytoplasm requires retrograde signaling from the intracellular Ca(2+) release machinery, a process that involves an intimate interaction between protein components on the intracellular and cell surface membranes. The cellular machinery that governs the Ca(2+) movement in muscle cells is developmentally regulated, reflecting maturation of the junctional membrane structure as well as coordinated expression of related Ca(2+) signaling molecules. Here we demonstrate the existence of SOCE in freshly isolated skeletal muscle cells obtained from embryonic days 15 and 16 of the mouse embryo, a critical stage of muscle development. SOCE in the fetal muscle deactivates incrementally with the uptake of Ca(2+) into the sarcoplasmic reticulum (SR). A novel Ca(2+)-dependent facilitation of SOCE is observed in cells transiently exposed to high cytosolic Ca(2+). Our data suggest that cytosolic Ca(2+) can facilitate SOCE whereas SR luminal Ca(2+) can deactivate SOCE in the fetal skeletal muscle. This cooperative mechanism of SOCE regulation by Ca(2+) ions not only enables tight control of SOCE by the SR membrane, but also provides an efficient mechanism of extracellular Ca(2+) entry in response to physiological demand. Such Ca(2+) signaling mechanism would likely contribute to contraction and development of the fetal skeletal muscle.