Correct skeletal muscle function is essential for coordinated movement. The foundations of the skeletal muscle system are established in the embryo. Our previous studies have demonstrated a role for nerve activity in the regulation of myofibril organisation during zebrafish embryogenesis [1]. Homozygous zebrafish embryos of the relaxed (red^ts25) mutant line are paralysed and die within days after hatching. The line carries a mutation in the β1a subunit of the voltage gated calcium channel, the dihydropyridine receptor, which is not expressed [2]. In the present study, we examined slow muscle fibre (adaxial cells) development in relaxed mutants, using whole mount immunocytochemistry. By 24 hours post fertilisation (hpf) adaxial cells had elongated and migrated to the lateral surface of the somite in both mutant and wild type embryos (n=4); a result indicative that calcium signalling via L-type calcium channel is not involved in these processes. In the wild type embryos the myofibrils are packed together into longitudinal bundles to form fibres, whilst in the mutant embryos myofibrils are not aligned laterally and appear disorganised. Previously we have shown that myofibril length was significantly increased relative to somite width in embryos from the nic1^b107 line, which carries a mutation in the α-subunit of the nicotinic acetylcholine receptor. Here we report an apparent increase in the myofibril length of relaxed mutants (1.06±0.04 n=12 at 24 hpf and 1.08±0.06 n=12 at 48 hpf) compared to wild type embryos (1.03±0.04 n=12 at 24 hpf and 1.06±0.03 n=12 at 48 hpf). We conclude that calcium signalling via dihydropyridine receptors has a role in myofibril organisation during embryogenesis.