The Ryanodine Receptor (RyR) intracellular calcium release channels (CRC) regulate release of calcium from intracellular stores in the ER/SR. Though expressed in many cell types, they are best known for their roles in muscle contraction; indeed loss-of-function mutations are associated with myopathy in humans. We propose this narrow view of the RyR function fails to account for the full range of phenotypes observed in humans carrying RYR1 mutations, which include slow muscle cell defects. Here we elucidate unexpected functions of RyR in the zebrafish embryo. Our lab has previously demonstrated multiple Hedgehog-dependent cell specification events, including generation of somite muscle cells and dorsal root ganglia, require RyR-mediated calcium mobilization. We report the results of our efforts to identify the specific combinations of ryr genes that support these developmental functions. We have i) reinvestigated the expression of ryr genes, ii) generated null ryr alleles, and iii) characterized phenotypes for single and compound mutants using a combination of histology, live imaging and behavioral assessments.