FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\stnB15
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General Information
Symbol
Dmel\stnB15
Species
D. melanogaster
Name
FlyBase ID
FBal0098642
Feature type
allele
Associated gene
Dmel\stnB
Associated Insertion(s)
Carried in Construct
Also Known As
stnC
Key Links
Genomic Maps

Allele class

loss of function allele

Mutagen
    Nature of the Allele
    Allele class

    loss of function allele

    (Fergestad et al., 1999)
    Mutagen
    Progenitor genotype
    Cytology
    Description

    No mutation is found in the stnA open reading frame (ORF) in "stnC" flies. An amino acid replacement resulting in a stop codon is found within the stnB ORF.

    (Kelly and Phillips, 2005)

    Nucleotide substitution: C?T.

    (Kelly and Phillips, 2005)

    Amino acid replacement: R415term.

    (Kelly and Phillips, 2005)
    Mutations Mapped to the Genome
    Curation Data
    Type
    Location
    Additional Notes
    References
    point_mutation
    X:22,990,660..22,990,660 [-]
    Nucleotide change:

    C22990660T

    Reported nucleotide change:

    C?T

    Amino acid change:

    R415term | stnB-PE; R415term | stnB-PF; R415term | stnB-PG; R394term | stnB-PH

    Reported amino acid change:

    R415term

    (Kelly and Phillips, 2005)
    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

        stnB15 mutant third instar larvae show defects in basal synaptic transmission, with a reduction in average excitatory junctional current (EJC) amplitude at neuromuscular junctions (muscle 6, segment 3) compared to controls. These larvae also show altered synaptic depression; when flies are exposed to high-frequency stimulation (HFS) at 10Hz the initial reduction in amplitude is less pronounced than in wild-type and recovery is also slower. A reduction in amplitude depression is also seen when flies are exposed to short trains of stimulation frequencies greater than or equal to 5Hz, and in response to paired stimuli with intervals of 25ms, 50ms or 100ms at high calcium levels. No difference is seen at low calcium concentrations.

        (Mohrmann et al., 2008)

        Mutant nmjs appear morphologically wild type though the nerve terminals are slightly smaller than normal. In electrophysiological recordings at the embryonic nmj nerve stimulation produces muscle contraction demonstrating that presynaptic depolarization evokes transmitter release and that muscle excitation-secretion response is intact. However evoked EJC peak amplitudes are significantly reduced and the release of neurotransmitter at mutant synapses is markedly asynchronous due to delayed presynaptic vesicle fusion. Mutants have an impaired ability to synchronously trigger calcium-mediated vesicle fusion. The overall level of neurotransmitter release is reduced. Variability in EJC peak amplitudes is increased approximately twofold, compared to wild type. Transmission fidelity is lost. Calcium sensitivity is unaltered. MEJC frequency is not significantly altered, though amplitude is increased, perhaps because of increased quantity of neurotransmitter in some vesicles. Mutant synapses exhibit severe fatigue after prolonged stimulation. Embryonic synapses show decreased synaptic vesicle density and accumulate membrane-recycling intermediates, though this defect is not apparent in mature larval nmjs.

        (Fergestad et al., 1999)
        External Data
        Interactions
        Show genetic interaction network for Enhancers & Suppressors
        Phenotypic Class
        Phenotype Manifest In
        Suppressed by
        Statement
        Reference

        stnA15, stnB15 has synaptic vesicle phenotype, suppressible by Scer\GAL44G/Syt1UAS.cLa

        (Fergestad and Broadie, 2001)
        Other
        Statement
        Reference

        stnA15, stnB15 has synaptic vesicle phenotype

        (Fergestad and Broadie, 2001)
        Additional Comments
        Genetic Interactions
        Statement
        Reference

        stnB15/Y ; Dap160EP2543/Df(2L)TW65 males show about 35% survival compared to control siblings. The surviving adults are sedentary, extremely uncoordinated and exhibit an extreme stress-sensitive phenotype. They die within 3 days of eclosion.

        (Kelly and Phillips, 2005)

        stnA15 stnB15 ("stnC") third instar larvae show a reduced mean excitatory junction potential (EJP) amplitude at the neuromuscular junction compared to wild-type larvae. The electroretinograms of stnA15 stnB15 ("stnC") animals lack on/off transients.

        (Estes et al., 2003)

        Third larval instar stnA15 stnB15 ("stnC") mutant larvae show reduced FM1-43 dye uptake (approximately 53 +/- 5% of control) at the neuromuscular junction after stimulus. The mutants show altered synaptic vesicle (SV) recycling and aberrant spatial localisation of vesicles within the synaptic boutons. The readily releasable vesicle pool is smaller than in wild type and although they are competent to fuse, they do so in a slower time course than normal. No difference in the rate of SV maturation is detectable. The mutants show a significantly delayed onset of endocytosis and a significantly smaller recycling SV pool after stimulus. Expression of sytScer\UAS.cLa under the control of Scer\GAL44G rescues the endocytotic functional defects seen in stnA15 stnB15 ("stnC") mutants.

        (Fergestad and Broadie, 2001)
        Xenogenetic Interactions
        Statement
        Reference
        Complementation and Rescue Data
        Comments

        Expression of the dicistronic P{UAS-stnAB.E} construct (which expresses stnAAB.Scer\UAS and stnBAB.Scer\UAS) under the control of Scer\GAL4elav-C155 rescues the mean excitatory junction potential (EJP) amplitude at the neuromuscular junction to wild-type in stnA15 stnB15 ("stnC") larvae. Expression of stnBScer\UAS.cEa under the control of Scer\GAL4elav-C155 rescues the mean excitatory junction potential (EJP) amplitude at the neuromuscular junction to wild-type in stnA15 stnB15 ("stnC") larvae. Expression of stnAScer\UAS.cEa under the control of Scer\GAL4elav-C155 does not rescue the mean excitatory junction potential (EJP) amplitude at the neuromuscular junction in stnA15 stnB15 ("stnC") larvae. Expression of stnBScer\UAS.cEa under the control of Scer\GAL4elav-C155 restores the on/off transients in the electroretinograms of stnA15 stnB15 ("stnC") animals. Expression of stnAScer\UAS.cEa under the control of Scer\GAL4elav-C155 does not restore the on/off transients in the electroretinograms of stnA15 stnB15 ("stnC") animals.

        (Estes et al., 2003)
        Images (0)
        Mutant
        Wild-type
        Stocks (1)
        Notes on Origin
        Discoverer

        Induced with: stnA15.

        (Fergestad et al., 1999)
        External Crossreferences and Linkouts ( 0 )
        Synonyms and Secondary IDs (2)
        References (7)