1.7kb deletion that almost entirely deletes the open reading frame, P-element insertion and flanking regulatory regions.
Neuronal expression of Syx1AScer\UAS.cBa under the control of Scer\GAL4elav-C155 in Syx1A3-69/Syx1AΔ229 results in a dramatic reduction in the frequency of constitutive secretion to 8.8Hz from 24.9Hz. The average amplitude of EPSPs is also significantly reduced in Syx1A3-69/Syx1AΔ229 mutants expressing Syx1AScer\UAS.cBa under the control of Scer\GAL4elav-C155. This EPSP amplitude is similar to that in Syx1AScer\UAS.cBa/Scer\GAL4elav-C155 flies, but significantly higher than wild-type.
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.
Syx1AΔ229/Syx1A[+] is an enhancer of visible phenotype of Scer\GAL4GMR.PF, bchsEP2299
Syx1AΔ229/Syx1A[+] is a suppressor of abnormal locomotor behavior | conditional phenotype of Hsap\HTT128Q.FL.UAS, Scer\GAL4C164
Syx1AΔ229/Syx1A[+] is a suppressor of abnormal neurophysiology phenotype of Hsap\HTT128Q.FL.UAS, Scer\GAL4elav-C155
Syx1AΔ229 is a suppressor of abnormal locomotor behavior | adult stage | progressive phenotype of Hsap\HTT128Q.1-336.UAS, Scer\GAL4elav.PU
Syx1AΔ229 is a suppressor of short lived phenotype of Hsap\HTT128Q.1-336.UAS, Scer\GAL4elav.PU
Syx1AΔ229 is a suppressor of visible phenotype of Hsap\HTT128Q.1-336.UAS, Scer\GAL4GMR.PU
Syx1AΔ229/Syx1A[+], Yif1doc-1 has visible | adult stage phenotype
Syx1AΔ229/Syx1A[+], Yif1doc-99 has partially lethal - majority die phenotype
Syx1AΔ229, smi26D1/smi26D[+] has abnormal smell perception | dominant | female phenotype
Syx1AΔ229, smi26D1 has abnormal smell perception | dominant | female phenotype
Syx1AΔ229/Syx1A[+] is an enhancer of eye phenotype of Scer\GAL4GMR.PF, bchsEP2299
Syx1AΔ229 is an enhancer of eye phenotype of αSnapUAS.cPa, Scer\GAL4GMR.PF
Syx1AΔ229/Syx1A[+] is a suppressor of rhabdomere of eye photoreceptor cell | conditional | adult stage phenotype of Hsap\HTT128Q.FL.UAS, Scer\GAL4GMR.PF
Syx1AΔ229/Syx1A[+] is a suppressor of ommatidium | adult stage phenotype of Hsap\HTT128Q.FL.UAS, Scer\GAL4GMR.PF
Syx1AΔ229 is a suppressor of eye phenotype of Hsap\HTT128Q.1-336.UAS, Scer\GAL4GMR.PU
Expression of SnapScer\UAS.cPa from the P{UAS-Snap.P}1 in a Syx1AΔ229 background results in an enhancement of the SnapScer\UAS.cPa phenotype in the eye, including increased necrosis around the perimeter of the compound eye and more dramatic furrowing at ommatidial junctions.
Syx1AΔ229/+ fully suppresses the increased excitatory junction potential (EJP) amplitude and decreased failure rate seen in Hsap\HD128Q.FL.Scer\UAS, Scer\GAL4elav-C155 animals at 0.25 mM Ca[2+].
Syx1AΔ229/+ suppresses the reduced number of rhabdomeres per ommatidium phenotype seen in Hsap\HD128Q.FL.Scer\UAS, Scer\GAL4GMR.PF animals at 20 days.
Syx1AΔ229/+ suppresses the external eye phenotype seen in Hsap\HD128Q.FL.Scer\UAS, Scer\GAL4GMR.PF animals.
Syx1AΔ229/+ suppresses the impaired motor performance, as measured by a climbing assay, of Hsap\HD128Q.FL.Scer\UAS, Scer\GAL4C164 animals.
Syx1AΔ229/+ reverses the increase in resting synaptic Ca[2+] levels at presynaptic terminals seen in Hsap\HD128Q.FL.Scer\UAS, Scer\GAL4elav-C155 larvae.
Syx1AΔ229/Syx1A3-69 is partially rescued by Scer\GAL4elav-C155/Syx1AUAS.cBa
Syx1AΔ229 is partially rescued by Syx1AA243V.V247A
Syx1AΔ229 is partially rescued by Syx1AI212A
Shows normal GABA staining in stage 17 nerve cord.