|Feature type||allele||Associated gene||Dmel\stnB|
|Also Known As||stnPH1|
|Allele class||loss of function allele|
|Mutagen||P-element activity, PM hybrid dysgenesis|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
Insertion into ORF2.
|Caused by insertion|
|Phenotype Manifest In|
stnA14 stnB14 "stnPH1" mutant embryos show a more than 90% reduction in FM1-43 dye uptake at the neuromuscular junction after stimulus compared to wild type.
Mutants die as mature embryos after a failure to hatch, due to lack of coordination. Mutant embryos show normal segmental patterning of the epidermis, muscles and nervous system. 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, 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. Synapses show decreased synaptic vesicle density and accumulate membrane-recycling intermediates.
|Phenotype Manifest In|
|Complementation & Rescue Data|
|Stocks ( 0 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 7 )|
|Secondary FlyBase IDs|
|References ( 11 )|
|Personal communication to FlyBase|