Homozygous embryos do not exhibit cuticle defects. Germline clones produce eggs with poorly differentiated cuticle.
Mutation compromises neurotransmission at the embryonic neuromuscular junction. Mature embryos fail to exhibit contraction waves but do emerge from the egg case. Cuticular structures are normal. Syx1A06737/Syx1A15ts transheterozygotes give progeny that exhibit reduced viability, rough eyes (disrupted ommatidial array, ommatidia may be missing, fused, improperly rotated or misaligned) and notching along the posterior margin of the wing. Clones cannot be recovered in the eye as lack of Syx1A activity in cells of the developing eye causes lethality.
Embryos do not exhibit typical peristaltic construction waves and reduced movements of the mouth hooks and muscles in the head region. Embryos were also unable to clear their tracheal system of fluid. Endogenous transmission is blocked but spontaneous vesicle release continues. The ability of vesicles to fuse and release neurotransmitter in response to calcium ion stimulus is impaired, reflected by the severely reduced excitatory junction current.