Mutants die at the late embryo/early first larval instar; a small minority of mutant larvae (less than 10%) hatch from the egg case but they all die during early to mid 1st instar. No gross morphological abnormalities are seen; the body plan appears fully differentiated and there are no defects in epidermal segmentation or patterning. The gut, tracheal system, musculature and nervous system appear fully differentiated with no detectable morphological abnormalities. Mutant neuromuscular junctions appear well differentiated with normally sized boutons and terminal size and number of boutons appears normal. Mutants show severe sluggishness, reduced endogenous locomotory movements and a lack of response to nose-touch. At a basal stimulation level, mean EJC amplitude at the embryonic neuromuscular junction (NMJ) is reduced by about 50% compared to controls. EJC amplitude is similarly reduced at higher stimulation frequencies. Frequency dependent depression is indistinguishable from controls. The coefficient of variation in EJC amplitude shows no significant difference from that of controls and there is no significant difference in long-term transmission maintenance in response to prolonged high frequency stimulation. The mutant NMJ shows decreased Ca²⁺ dependence relative to controls. The mean mEJC amplitude and distribution of mEJC amplitudes of mutant NMJs is similar to wild type. There is a significant accumulation of synaptic vesicles at active zones at the mutant embryonic NMJ. The average density of dense core vesicles throughout the NMJ bouton is significantly increased relative to controls.

Cadps^BJ has lethal | recessive phenotype, suppressible by Rnor\Cadps^UAS.cRa/Scer\GAL4^e22c

Cadps^BJ has neuromuscular junction phenotype, non-suppressible by Scer\GAL4^eve.RKK/Rnor\Cadps^UAS.cRa