During muscle contraction, Ca2+ released from the sarco(endo)plasmic reticulum (SER) into the cytosol activates actin/myosin sliding. It is then rapidly pumped out of the cytosol by the SER Ca2+ ATPase 1 (SERCA1) to allow muscle relaxation. On p. 5457, Hirata and colleagues report that this muscle relaxation does not occur in the zebrafish behavioural mutant accordion (acc). Twenty-four hours post-fertilisation, zebrafish embryos respond to touch by rapidly coiling their tails once each way; acc mutant embryos respond with a bilateral contraction of trunk muscles, which shortens their trunks. Although nerve transmission is normal in these mutants, the cytosolic Ca2+decay in their muscles is very slow, preventing their muscles from relaxing normally. This defect is due to a mutation in the atp2a1 gene, which encodes SERCA1, making the acc mutant an attractive model in which to study Brody disease, a human motor disorder caused by SERCA1mutations.