Allele Dmel\scramb2^Δ57

General Information
Symbol	Dmel\scramb2^Δ57	Species	D. melanogaster
Name		FlyBase ID	FBal0212828
Feature type	allele	Associated gene	Dmel\scramb2

Allele class	loss of function allele
Mutagen	ethyl methanesulfonate
Recent Updates
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FB2013_03
FB2013_02
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Nature of the Allele
Allele class	loss of function allele (Acharya et al., 2006)
Mutagen	ethyl methanesulfonate (Acharya et al., 2006)
Mutations Mapped to the Genome

Type Location Additional Notes References
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype
Nature of the lesion	Statement Reference A T-to-A transition at the first exon-intron junction leads to termination of the gene after 57 amino acids. (Acharya et al., 2006) Nucleotide substitution: T?A. (Acharya et al., 2006)
Cytology
Phenotypic Data
Phenotypic Class
	viable (Acharya et al., 2006)
Phenotype Manifest In

Detailed Description
	Statement Reference scramb2^Δ57 mutants are viable and fertile and don't exhibit any developmental defects. scramb2^Δ57 single mutant synapses display transmitter release and plasticity properties that do not differ significantly from control. The immune competence of homozygous scramb2^Δ57 mutants is similar to wild-type flies and not compromised (as measured by survival rates after infection with mixed microorganisms). (Acharya et al., 2006)
External Data
Linkouts
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Statement Reference scramb1^Δ38, scramb2^Δ57 has neurophysiology defective phenotype, suppressible by Scer\GAL4^elav-C155/scramb2^{Scer\UAS.T:Avic\GFP} (Acharya et al., 2006) scramb1^Δ38, scramb2^Δ57 has neurophysiology defective phenotype, suppressible by scramb1^Scer\UAS.cAa/Scer\GAL4^Act.PU (Acharya et al., 2006)
Other
Statement Reference scramb1^Δ38, scramb2^Δ57 has hyperactive phenotype (Acharya et al., 2006) scramb1^Δ38, scramb2^Δ57 has neurophysiology defective phenotype (Acharya et al., 2006)
Phenotype Manifest In
Suppressed by
Statement Reference scramb1^Δ38, scramb2^Δ57 has presynaptic active zone phenotype, suppressible by scramb1^Scer\UAS.cAa/Scer\GAL4^Act.PU (Acharya et al., 2006) scramb1^Δ38, scramb2^Δ57 has synaptic vesicle phenotype, suppressible by scramb1^Scer\UAS.cAa/Scer\GAL4^Act.PU (Acharya et al., 2006)
Other
Statement Reference scramb1^Δ38, scramb2^Δ57 has presynaptic active zone phenotype (Acharya et al., 2006) scramb1^Δ38, scramb2^Δ57 has synaptic vesicle phenotype (Acharya et al., 2006)
Additional Comments
Genetic Interactions
Statement Reference The immune competence of scramb1^Δ38/scramb2^Δ57 trans-heterozygous mutants is similar to wild-type flies and not compromised (as measured by survival rates after infection with mixed microorganisms). scramb1^Δ38/scramb2^Δ57 double mutant flies appear visibly more active compared to either single mutants or control flies. scramb1^Δ38/scramb2^Δ57 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 scramb1^Δ38/scramb2^Δ57 double mutant presynaptic terminals. The time course of decline of FM1-4 fluorescence brightness is similar in scramb1^Δ38/scramb2^Δ57 double mutant and control boutons, indicating similar properties of ECP exocytosis. The rate of reserve pool recruitment of synaptic vesicles is markedly enhanced in scramb1^Δ38/scramb2^Δ57 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 scramb1^Δ38/scramb2^Δ57 double mutants can be rescued to control levels through the expression of scramb1^Scer\UAS.cAa under the control of Scer\GAL4^Act. Reserve pool recruitment of synaptic vesicles in scramb1^Δ38/scramb2^Δ57 double mutant larvae is rescued to control levels through the expression of scramb1^Scer\UAS.cAa under the control of Scer\GAL4^Act. Synaptic transmission in scramb1^Δ38/scramb2^Δ57 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 scramb1^Scer\UAS.cAa (under the control of Scer\GAL4^Act). 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 scramb1^Scer\UAS.cAa in the double mutant resuces post-terminal potentiation to normal. Expression of scramb2^{Scer\UAS.T:Avic\GFP} (under the control of Scer\GAL4^elav-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. (Acharya et al., 2006)
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Comments
Stocks ( 0 )

Notes on Origin
Discoverer

External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 1 )
Reported As
Symbol Synonym	scramb2^Δ57
Name Synonym
Secondary FlyBase IDs

References ( 1 )
Research paper	Acharya et al., 2006, J. Cell Biol. 173(1): 69--82 Drosophila melanogaster Scramblases modulate synaptic transmission. [FBrf0190926]

Allele Dmel\scramb2Δ57

Allele Dmel\scramb2^Δ57