FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\Syt1AD1
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General Information
Symbol
Dmel\Syt1AD1
Species
D. melanogaster
Name
FlyBase ID
FBal0032844
Feature type
allele
Associated gene
Dmel\Syt1
Associated Insertion(s)
Carried in Construct
Key Links
Genomic Maps

Allele class
Mutagen
Nature of the Allele
Allele class
Mutagen
ethyl methanesulfonate
(DiAntonio and Schwarz, 1994, Littleton et al., 1994, DiAntonio et al., 1993)
Progenitor genotype
Cytology
Description

The premature stop codon is between the two C2 domains.

(DiAntonio and Schwarz, 1994)

Amino acid replacement: W311term.

(DiAntonio and Schwarz, 1994)
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
point_mutation
2L:2,792,232..2,792,232 [-]
Nucleotide change:

G2792232A

Reported nucleotide change:

G?A

Amino acid change:

W311term | Syt1-PA; W309term | Syt1-PB; W309term | Syt1-PC; W311term | Syt1-PE; W311term | Syt1-PG; W311term | Syt1-PH; W309term | Syt1-PI

Reported amino acid change:

W311term

Comment:

G to A nucleotide change at the second or third position of the Trp codon leads to a nonsense mutation (exact site of mutation unspecified). Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

(Broadie et al., 1994)
Variant Molecular Consequences
Associated Sequence Data
DDBJ / EMBL / GenBank
DNA sequence
Protein sequence
 
UniProtKB/Swiss-Prot
    UniProtKB/TrEMBL
      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 )
       
      Disease-implicated variant(s)
       
      Phenotypic Data
      Phenotypic Class
      Phenotype Manifest In
      Detailed Description
      Statement
      Reference

      Syt1AD1/Syt1T7 synapses (which lack the C[[2]]B domain) exhibit decreased evoked neurotransmitter release compared to wild-type controls.

      (Poskanzer et al., 2006)

      sytAD1/sytN13 mutants show synchronous release following stimulation of the neuromuscular junction, although it is greatly reduced compared to controls. The cooperative Ca2+ dependence of synchronous release is abolished. Although the absolute number of asynchronous release events is reduced in sytAD1/sytN13 mutants, the time constant for the remaining delayed release events is unchanged. The total number of vesicles release during repetitive stimulation at the sytAD1/sytN13 neuromuscular junction is reduced approximately twofold compared to wild type, but the quantal content is reduced more than 100-fold. The frequency of spontaneous miniature synaptic currents at the embryonic sytAD1/sytN13 neuromuscular junction is not increased compared to wild type. The quantal content of nerve evoked release at the neuromuscular junction is reduced in heterozygotes compared to controls.

      (Yoshihara and Littleton, 2002)

      sytAD1/sytT41 mutants lack the on-off transients normally seen during electroretinogram recordings in the retina. There is a decrease in the overall number of synaptic vesicles at the photoreceptor synapses in sytAD1/sytT7 and sytAD1/sytT41 mutants.

      (Littleton et al., 2001)

      sytAD1/sytT41 transheterozygotes survive until eclosion. The frequency of immature filopodial contacts on muscle fibres 6 and 7 ("collateral sprouts") in sytAD1/sytT41 embryos is similar to wild-type.

      (Jarecki and Keshishian, 1995)

      Rare survivors when transheterozygotes with Df(2L)DTD2 are recovered.

      (DiAntonio and Schwarz, 1994)

      Transheterozygote combinations with other syt alleles are lethal, but there are some adult survivors with sytT7 and sytT41.

      (Littleton et al., 1994)

      Sluggish crawling and feeding behaviour. Larvae do not grow or moult as wild type larvae would, and die after a week (at 18oC).

      (DiAntonio et al., 1993)
      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
      Rescued by

      Df(2L)DTD2/Syt1AD1 is rescued by Syt1elav.PD

      (DiAntonio and Schwarz, 1994)
      Partially rescued by

      Syt1AD1 is partially rescued by Syt1elav.PD

      (DiAntonio and Schwarz, 1994)
      Comments

      Homozygous lethality can be rescued by sytelav.PD. Rescued flies that emerge are lethargic and show an electrophysiological deficit due to insufficient syt. A second copy of sytelav.PD improves viability and motor activity. ERGs of mutants carrying one copy of sytelav.PD lack both on- and off-transients suggesting a disruption in synaptic communication. sytAD1/Df(2L)DTD2; sytelav.PD/+ individuals are more robust than the rescued null alleles: they fly more and climb up the sides of the vial more quickly after being tapped to the bottom. In mutants the evoked neurotransmitter release is decreased and spontaneous release in increased (intracellular recordings made from muscle 6).

      (DiAntonio and Schwarz, 1994)
      Images (0)
      Mutant
      Wild-type
      Stocks (0)
      Notes on Origin
      Discoverer
      Comments
      Comments

      Mutant phenotype can be rescued, when homozygous or in trans to sytN6, by sytelav.PD.

      (Littleton et al., 1994)
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (2)
      Reported As
      Symbol Synonym
      Syt1AD1
      (Poskanzer et al., 2006)
      sytAD1
      Name Synonyms
      Secondary FlyBase IDs
        References (8)