Homozygous mutant embryos fail to secrete cuticle, denticle belts and mouthhooks. Gut and ventral nerve cord development are grossly abnormal.
The oocyte accumulates vacuoles at later stages.
Heterozygotes with Syx1A3-69 show paralysis after a few seconds at 38oC.
Homozygotes exhibit complete blockade of all forms of neurotransmitter release. Incomplete compaction of the ventral nerve cord is observed. Late stage embryos exhibit incomplete fasciculation of the intersegmental and segmental nerve bundles and the longitudinal tracts. Also nonneural forms of secretion are impaired, yolk digestion in the gut is abnormal and several layers of the cuticle are missing. Syx1AΔ229/Syx1A15ts transheterozygotes produce 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. Germline clones produce viable oocytes but are rudimentary and do not produce eggs. Clones cannot be recovered in the eye as lack of Syx1A activity in cells of the developing eye causes lethality.
Paralysis and embryonic lethality results. Evoked synaptic transmission is completely eliminated at the NMJ. However the postsynaptic membrane responds normally to applied L-glutamate. The NMJs develop in the normal synaptic domains on muscles, and bouton morphology is normal at the light microscope level. Bouton number is reduced by 30-50%. Ultrastructure of embryonic synapses is largely indistinguishable from wild type. The percentage of vesicles that have contacted, or are close to, the presynaptic membrane is increased compared to wild type. At both NMJs and central synapses there is an unusual abundance of enlarged vesicles. Miniature excitatory junctional currents do not occur at the mature embryonic NMJ, though increased saline osmolarity can trigger mass exocytosis, as in wild type, demonstrating that the docked vesicles are mature and functional. Latrotoxin-induced fusion of synaptic vesicles fails.
Embryos fail to secrete most or all cuticle, gut is morphologically abnormal and the yolk in the gut is undigested. Condensation of the CNS is incomplete. Subtle defects in axonal morphology and fasciculation, axon bundles of the intersegmental and segmental nerves appear thickened and irregular in shape. Neuromuscular architecture is relatively normal.