Syx1A continues to be abundantly expressed in the nurse cell membranes of egg chambers during stages 1-8, and Syx1A levels fade during stages 8 and 9. Syx1A protein is present in the adult brain and the synaptic substations of the visual system. Syx1A is concentrated in the neuropil regions of the brain and is somewhat enriched at synaptic regions, such as in the lamina and medulla of the optic lobes where photoreceptor axons form synaptic contacts with second order neurons. Unhatched embryos were examined 30-36 hr after egg lay. Mutant embryos do not exhibit typical peristaltic contraction waves, which allow normal embryos to hatch from the egg case, and they display only very reduced movements of the mouth hooks and muscles in the head region.
Embryos are unable to clear their tracheal system of fluid.
Complete absence of syx1A causes subtle morphological defects in the peripheral and central nervous systems, affects nonneural secretory events, and entirely abolishes neurotransmitter release. Null mutant embryos fail to secrete most or all cuticle, the gut is morphologically abnormal, and yolk in the gut is undigested. However, the Malpighian tubules secrete uric acid, and the lumen of the salivary glands contains glue proteins, unlike mutants for rop that show more severe secretory and developmental defects. In addition, the severe muscle and CNS defects seen in rop mutants are not present in syx1A mutants. Axon bundles of the intersegmental and segmental nerves appear thickened and irregular in shape in syx1A mutants.