|Feature type||allele||Associated gene||Dmel\Dys|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
Dys[E6] lacks the DLP2 muscle-specific isoform but expresses the Dp186 isoform at wild-type levels.
|Caused by aberration|
|Phenotype Manifest In|
Most of the posterior crossvein is missing in homozygous Dys[E6] mutants. The remnant of the posterior crossvein is detached, it does not reach the fourth and fifth longitudinal wing veins. The posterior crossvein appears normal in Dys[E6] heterozygotes. Dys[E6]/Dys[det-1] heterozygotes display posterior crossvein abnormalities. There is an increase in the number of T-bars at Dys[E6] mutant neuromuscular junctions relative to controls. Quantal content (QC) at the third larval neuromuscular junction is increased in Dys[E6]/+ heterozygotes relative to wild-type controls.
Synaptic currents in Dys[E6] are no different in amplitude compared with wild-type. Evoked synaptic currents at the neuromuscular junction are, however, significantly elevated.
Dys[E6]/Df(3R)Dl-X43 mutant ovaries show oocyte polarity defects. Dys[8-2]/Dys[E6] mutant third instar larval eye discs develop aberrant neuronal projections from photoreceptor neurons to the brain optic lobes. Axons stop irregularly, making gaps in the normal termination zone of the lamina plexus, deviating from the path and bundling aberrantly. This axon projection phenotype not observed in Dys[8-2]/+ mutant discs.
DysE6 mutant larvae do not display statistically significant differences in muscle size, number of boutons, lengths of the synaptic termini, and the number of terminal branches, compared to wild-type controls. EJP amplitudes, evoked by nerve stimulation at 0.3Hz are approximately 45% increased in DysE6 mutants compared with control larvae, due to an increase in presynaptic glutamate release in the mutants. Spontaneous mEJP amplitudes are essentially unchanged in the mutants compared to controls. Quantal content is approximately 50-65% higher in DysE6 mutants compared to wild-type. The frequency of spontaneous neurotransmitter release is elevated approximately 35-50% in DysE6 mutants. DysE6/DysGE20705 trans-heterozygotes exhibit an increase in EJP amplitude compared to controls when evoked by nerve stimulation at 0.3Hz. Quantal content is also significantly higher in DysE6/DysGE20705 trans-heterozygotes compared to wild-type. DysE6/+ heterozygotes exhibit an increase in EJP amplitude compared to controls when evoked by nerve stimulation at 0.3Hz. Quantal content is also significantly higher in DysE6/+ trans-heterozygotes compared to wild-type. Ca2+ cooperativity at DysE6 mutant neuromuscular junctions is the same as in the wild-type. Synaptic boutons in DysE6 appear slightly more elongated than in controls. The areas of the bouton occupied by vesicles is increase in DysE6 mutants compared with wild-type. The number of active zones with a T-bar relative to the total number of active zones is significantly increased in DysE6 mutants by approximately two-fold, whereas the overall number of active zones does not increase.
|NOT suppressed by|
|Phenotype Manifest In|
|NOT suppressed by|
Most of the posterior crossvein is missing in Dys[E6]/+, cv-c/+ double heterozygotes. The remnant of the posterior crossvein is detached, it does not reach the fourth and fifth longitudinal wing veins. The increased quantal content (QC) measured at the neuromuscular junction of Dys[E6]/+ mutants is not reduced as a result of expression of cv-c[Scer\UAS.cDa] under the control of Scer\GAL4[G14]. Heterozygosity for Cdc42 in a Dys[E6]/+ mutant background restores quantal content (QC) to wild-type levels.
|Complementation & Rescue Data|
|Not rescued by|
|Stocks ( 0 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 4 )|
|Secondary FlyBase IDs|
|References ( 4 )|