Homozygous embryos exhibit incomplete dorsal migration of the lateral epidermis and failure of dorsal epidermal closure. CNS and neuromusculature appear morphologically normal and the mutant embryos exhibit coordinated muscle movements similar to those observed in wild-type locomotion. Synaptogenesis at the neuromuscular junction (NMJ) is largely normal. Embryos also exhibit near normal physiological development and basal excitation-secretion function at the NMJ. The amplitude and frequency of endogenous excitatory junctional currents (EJCs) is reduced relative to wild type. This reduced function originates in a presynaptic defect, basal presynaptic function is mildly impaired. MEJC (miniature EJCs) amplitude is not altered. NMJ exhibits a transmission defect, the calcium dependence curve is shifted to the right indicating a higher level of external calcium is required to achieve the given level of secretion. Synaptic transmission fidelity and fatigue resistance properties are impaired. Short-term facilitation is strengthened but synaptic augmentation an potentiation are disrupted.