The calcium (Ca²⁺) signals that help regulate skeletal muscle development and differentiation consist of a complex interaction of excitation-transcription coupling and excitation-contraction coupling, where both forms of signaling appear to be necessary to generate anatomically normal and functional muscle. The challenge when exploring, modulating, and visualizing these Ca²⁺ signals, lies in both their spatial and temporal nature, as well as the variety of Ca²⁺ mobilizing agents and channels/ receptors that come into play. The latest agonist/ receptor pair that has been reported to be involved in muscle differentiation is nicotinic acid adenine dinucleotide phosphate (NAADP) and Two-pore channels (TPCs), respectively, where NAADP has been shown to be the most potent intracellul...[ Read more ]

The calcium (Ca²⁺) signals that help regulate skeletal muscle development and differentiation consist of a complex interaction of excitation-transcription coupling and excitation-contraction coupling, where both forms of signaling appear to be necessary to generate anatomically normal and functional muscle. The challenge when exploring, modulating, and visualizing these Ca²⁺ signals, lies in both their spatial and temporal nature, as well as the variety of Ca²⁺ mobilizing agents and channels/ receptors that come into play. The latest agonist/ receptor pair that has been reported to be involved in muscle differentiation is nicotinic acid adenine dinucleotide phosphate (NAADP) and Two-pore channels (TPCs), respectively, where NAADP has been shown to be the most potent intracellular Ca²⁺ mobilizing agent described to date. Here I present new data that describes what appears to be a complex relationship between Ca²⁺ released via TPC2, and that via the other two well-known intracellular Ca²⁺ mobilizing receptors, ryanodine receptors (RyRs) and inositol trisphosphate receptors (IP₃Rs). Furthermore, I show how this interaction appears to be necessary for normal slow muscle development in the trunk of segmentation period zebrafish, as well as subsequent contractile activity manifested as initial spontaneous trunk coiling followed by burst-swimming behavior.