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General Information
Symbol
Dmel\Syx1AH3-C
Species
D. melanogaster
Name
FlyBase ID
FBal0099813
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Carried in construct
Cytology
Nature of the lesion
Statement
Reference

A deletion removes the highly basic C-terminal 14 amino acids of the H3 domain.

Allele components
Product class / Tool use(s)
Regulatory region(s)
Encoded product / tool
Expression Data
Reporter Expression
Additional Information
Statement
Reference
 
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

In contrast with wild-type, Syx1AΔ229 and Syx1A06737 flies rescued with Syx1AH3-C, undergo no peristaltic muscle contractions prior to hatching, and show a poor response to tactile stimulation. Syx1AΔ229 embryos rescued with Syx1AH3-C appear thinner and somewhat irregular compared to wild-type, though cuticle is secreted normally. Using whole-cell patch-clamp analysis, about 70% of Syx1AH3-C mutants in a Syx1AΔ229 null background show an evoked neurotransmission that is strongly reduced when compared to wild-type. In the remainder, the evoked response is abolished. Mutants reveal robust postsynaptic responses, similar to controls. mEJC frequency is also significantly increased as compared to controls. Mutants exhibit a decreased reliability of excitation-secretion coupling: evoked neurotransmission in these mutants is characterised by asynchronous release, low fidelity of release, a high failure rate and increased variability of response. This suggests defects in the ability of the fusion machinery to properly regulate synchronized release of synaptic vesicles in response to Ca2+ influx.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference
Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Partially rescues
Fails to rescue
Comments
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
Reported As
Symbol Synonym
Syx1AH3-C
syx1AH3-C
Name Synonyms
Secondary FlyBase IDs
    References (1)