|Feature type||allele||Associated gene||Dmel\scramb2|
|Allele class||loss of function allele|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
A T-to-A transition at the first exon-intron junction leads to termination of the gene after 57 amino acids.
Nucleotide substitution: T?A.
|Phenotype Manifest In|
scramb2Δ57 mutants are viable and fertile and don't exhibit any developmental defects. scramb2Δ57 single mutant synapses display transmitter release and plasticity properties that do not differ significantly from control. The immune competence of homozygous scramb2Δ57 mutants is similar to wild-type flies and not compromised (as measured by survival rates after infection with mixed microorganisms).
scramb1Δ38, scramb2Δ57 has neurophysiology defective phenotype, suppressible by Scer\GAL4elav-C155/scramb2Scer\UAS.T:Avic\GFP
|Phenotype Manifest In|
scramb1Δ38, scramb2Δ57 has presynaptic active zone phenotype, suppressible by scramb1Scer\UAS.cAa/Scer\GAL4Act.PU
The immune competence of scramb1Δ38/scramb2Δ57 trans-heterozygous mutants is similar to wild-type flies and not compromised (as measured by survival rates after infection with mixed microorganisms). scramb1Δ38/scramb2Δ57 double mutant flies appear visibly more active compared to either single mutants or control flies. scramb1Δ38/scramb2Δ57 double mutant larval neuromuscular junctions exhibit a significant increase in the number of synaptic vesicles and more vesicles docked at the active zone. The single mutants, on the other hand, do not show significant changes in the ultrastructure of neuromuscular junctions, except that there are more than one docked vesicle at the active zone of most of the type 1b boutons examined. FM1-43 dye loading studies indicate an excess content of synaptic vesicles in scramb1Δ38/scramb2Δ57 double mutant presynaptic terminals. The time course of decline of FM1-4 fluorescence brightness is similar in scramb1Δ38/scramb2Δ57 double mutant and control boutons, indicating similar properties of ECP exocytosis. The rate of reserve pool recruitment of synaptic vesicles is markedly enhanced in scramb1Δ38/scramb2Δ57 double mutant boutons, as indicated by a significantly faster rate of fluorescence brightness decline. The extent of fluorescence decline induced by a 5-min stimulation of the nerve at 0.5Hz in the double mutant is also significantly enhanced relative to control. These results reveal that reserve pool recruitment in double-mutant synapse is abnormally enhanced. The extent of FM1-43 dye loading in scramb1Δ38/scramb2Δ57 double mutants can be rescued to control levels through the expression of scramb1Scer\UAS.cAa under the control of Scer\GAL4Act. Reserve pool recruitment of synaptic vesicles in scramb1Δ38/scramb2Δ57 double mutant larvae is rescued to control levels through the expression of scramb1Scer\UAS.cAa under the control of Scer\GAL4Act. Synaptic transmission in scramb1Δ38/scramb2Δ57 double mutants differed in several aspects from the control. The frequency of spontaneous postsynaptic currents is signficantly enhanced in the double mutant. Release probability, quantal content, and nerve-evoked postsynaptic currents are significantly larger in the double mutant. On the other hand, the amplitude of current and the charge transferred by the release of a single quantum, are the same as in controls. The Ca2+ cooperativity coefficient is similar in double mutants as controls. However, in double mutant synapses, the curve is shifted toward lower Ca2+ concentrations. Neurotransmitter release evoked by application of a 20 second hyperosmotic shock in the vicinity of the synapse is dramatically increased in the double mutant. The synaptic defects in the double mutant are rescued by the introduction of scramb1Scer\UAS.cAa (under the control of Scer\GAL4Act). Analysis of paired-pulse faciliation reveals that, although the extent of facilitation of neurotransmitter release in the double mutant is dimished relative to the control, this difference is not significantly different from the control. The extent of facilitation of transmitter release elicited by high-frequency stimulation of the nerve did not differ significantly from the control. On the other hand, post-terminal potentiation in the double mutant is abnormally prolonged. Transmitter release remains significantly potentiated after 100 seconds in the double mutant, compared to a return to values before stimulation after ~50 seconds in controls. Introduction of scramb1Scer\UAS.cAa in the double mutant resuces post-terminal potentiation to normal. Expression of scramb2Scer\UAS.T:Avic\GFP (under the control of Scer\GAL4elav-C155) resuces the content of ECP, RP, mobilisation of RP pool of vesicles, postsynaptic current amplitude, quantal content, tetanic facilitation, and post-tetantic facilitation to control levels.
|Complementation & Rescue Data|
|Stocks ( 0 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 1 )|
|Secondary FlyBase IDs|
|References ( 1 )|