Large somatic clones of Ace^j50 homozygous cells in the developing retina of late third instar larvae do not disrupt ommatidial development but lead to photoreceptor axon guidance defects: mutant axons wander significantly from their normal paths and/or cross over aberrantly. This effect shows some non-autonomy, as wild-type axons in their vicinity are also mistargeted. However, mistargeted axons do not extend into the medulla target field. Axons of mutant photoreceptors reaching the lamina plexus fail to arborize.

Ace^j50 embryos show rapid and uncoordinated peristalsis. The synaptic currents of aCC and RP2 Ace^j50 mutant neurons are smaller and more numerous than in wild type. Additionally there is a significant depolarization of resting membrane potential. The ability of aCC/RP2 to fire action potentials (APs) in response to an injection of constant current is decreased in Ace^j50 mutants compared to Ace^j50/+ heterozygotes and the duration between successive APs is increased. Voltage-clamp analysis of aCC/RP2 neurons shows a significant reduction in peak current density of voltage-dependent inward Na⁺ current in Ace^j50 mutants compared to wild type. There is an increase in the amount of current required to fire an equal number of APs following treatment with tetrodotoxin, although this is less marked than in wild-type.

Ace^j40/Ace^j50 second and third instar larvae which have been raised at 18^oC are no more susceptible to heat-induced paralysis when exposed to 38^oC than control larvae, and are if anything, less adversely affected.

Ace^j40/Ace^j50 adults which have been raised at 18^oC show a slight defects in phototactic behaviour when tested at 18^oC. The defects in phototaxis increase if the flies are subjected to 29^oC.

Ace^j40/Ace^j50 adults which have been raised at 18^oC but subjected to a heat pulse during pupal development show severely defective phototaxis, while heat treatment during larval development results in only a slight decrement in phototaxis in the resulting adults.

Ace^j40/Ace^j50 adults which have been raised at 18^oC but subjected to a heat pulse during pupal development show a severe reduction in general locomotor activity compared to mutant adults of the same genotype that have been maintained at 18^oC throughout development.

Ace^j40/Ace^j50 adults which have been raised at 18^oC and then shifted to 29^oC for 11 days show defects in the neuropile of the brain; it appears compacted and disorganised compared to wild type.

Ace^j50 has abnormal neurophysiology | dominant phenotype, suppressible by Pka-R1^BDK.UAS/Scer\GAL4^eve.RN2O

Ace^j50 has abnormal neurophysiology | dominant phenotype, suppressible by dnc^UAS.cCa/Scer\GAL4^eve.RN2O