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General Information
D. melanogaster
FlyBase ID
Feature type
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
syxΔ229, syx229, Df(3R)Δ229
Key Links
Nature of the Allele
Mutations Mapped to the Genome
Additional Notes
Associated Sequence Data
DNA sequence
Protein sequence
Nature of the lesion

1.7kb deletion that almost entirely deletes the open reading frame, P-element insertion and flanking regulatory regions.

Excision of the P-element resulting in a 2.0kb deletion removing all of Syx1A.

Expression Data
Reporter Expression
Additional Information
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Modifiers Based on Experimental Evidence ( 1 )
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
Disease-implicated variant(s)
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description

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.

External Data
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Enhancer of
Suppressor of
Additional Comments
Genetic Interactions

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.

Xenogenetic Interactions

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.

Complementation and Rescue Data
Partially complements
Not rescued by

Lethality is rescued by one copy of the Syx1A+t11 or Syx1A+t6 constructs, rescued adults are viable, fertile and morphologically normal. 11%-22% Syx1AΔ229/Syx1A177 transheterozygous adults are viable.

Images (0)
Stocks (2)
Notes on Origin

Shows normal GABA staining in stage 17 nerve cord.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (12)
References (24)