Allele Dmel\Dys^E6

General Information
Symbol	Dmel\Dys^E6	Species	D. melanogaster
Name		FlyBase ID	FBal0216501
Feature type	allele	Associated gene	Dmel\Dys

Allele class
Mutagen	P-element activity
Recent Updates
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FB2013_03
FB2013_02
All updates	Click here to see a list of all updates to this record from FB2010_08 and on.
Nature of the Allele
Allele class
Mutagen	P-element activity (van der Plas 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	Dys^EP3397 (van der Plas et al., 2006)
Nature of the lesion	Statement Reference Dys[E6] lacks the DLP2 muscle-specific isoform but expresses the Dp186 isoform at wild-type levels. (Fradkin et al., 2008) A deletion of 2.7kb caused by the imprecise excision of P{EP}Dys^EP3397 removes genomic sequences encoding all of the DLP2 5' untranslated region and extends ~200bp downstream of the DLP2 intiator ATG but does not delete the unique DLP1 first exon. (van der Plas et al., 2006)
Caused by aberration	Df(3R)Dys^E6 (van der Plas et al., 2006)
Cytology
Phenotypic Data
Phenotypic Class
	cell polarity defective (with Df(3R)Dl-X43) (Shcherbata et al., 2007) neuroanatomy defective \| third instar larval stage (with Dys^8-2) (Shcherbata et al., 2007) neurophysiology defective (van der Plas et al., 2006, Fradkin et al., 2008) neurophysiology defective (with Dys^GE20705) (van der Plas et al., 2006) neurophysiology defective \| dominant (Pilgram et al., 2011) visible (with Dys^det-1) (Pilgram et al., 2011) visible \| recessive (Pilgram et al., 2011)
Phenotype Manifest In
	eye disc \| third instar larval stage (with Dys^8-2) (Shcherbata et al., 2007) eye photoreceptor cell \| third instar larval stage (with Dys^8-2) (Shcherbata et al., 2007) lamina plexus \| third instar larval stage (with Dys^8-2) (Shcherbata et al., 2007) neuromuscular junction (Pilgram et al., 2011) oocyte (with Df(3R)Dl-X43) (Shcherbata et al., 2007) posterior crossvein (Pilgram et al., 2011) posterior crossvein (with Dys^det-1) (Pilgram et al., 2011) presynaptic active zone (van der Plas et al., 2006) t-bar (Pilgram et al., 2011) terminal bouton (van der Plas et al., 2006)
Detailed Description
	Statement Reference 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. (Pilgram et al., 2011) 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. (Fradkin et al., 2008) 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. (Shcherbata et al., 2007) Dys^E6 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 Dys^E6 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 Dys^E6 mutants compared to wild-type. The frequency of spontaneous neurotransmitter release is elevated approximately 35-50% in Dys^E6 mutants. Dys^E6/Dys^GE20705 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 Dys^E6/Dys^GE20705 trans-heterozygotes compared to wild-type. Dys^E6/+ 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 Dys^E6/+ trans-heterozygotes compared to wild-type. Ca²⁺ cooperativity at Dys^E6 mutant neuromuscular junctions is the same as in the wild-type. Synaptic boutons in Dys^E6 appear slightly more elongated than in controls. The areas of the bouton occupied by vesicles is increase in Dys^E6 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 Dys^E6 mutants by approximately two-fold, whereas the overall number of active zones does not increase. (van der Plas et al., 2006)
External Data
Linkouts
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
NOT suppressed by
Statement Reference Dys^E6 has neurophysiology defective \| dominant phenotype, non-suppressible by Scer\GAL4^G14/cv-c^Scer\UAS.cDa (Pilgram et al., 2011)
Other
Statement Reference Dys^E6, cv-c¹ has visible \| dominant phenotype (Pilgram et al., 2011)
Phenotype Manifest In
NOT suppressed by
Statement Reference Dys^E6 has neuromuscular junction phenotype, non-suppressible by Scer\GAL4^G14/cv-c^Scer\UAS.cDa (Pilgram et al., 2011)
Additional Comments
Genetic Interactions
Statement Reference Most of the posterior crossvein is missing in Dys[E6]/+, cv-c[1]/+ 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[4] in a Dys[E6]/+ mutant background restores quantal content (QC) to wild-type levels. (Pilgram et al., 2011)
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Rescued by	Dys^E6 is rescued by Scer\GAL4^G14/Dys^GS12472 (van der Plas et al., 2006)
Not rescued by	Dys^E6 is not rescued by Scer\GAL4^Rapgap1-OK6/Dys^GS12472 (van der Plas et al., 2006)
Comments
Stocks ( 0 )

Notes on Origin
Discoverer

External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 4 )
Reported As
Symbol Synonym	det^E6 dys^E6 (van der Plas et al., 2006) Dys^E6 (Fradkin et al., 2008, Pilgram et al., 2011) Dys^e6 (Shcherbata et al., 2007)
Name Synonym
Secondary FlyBase IDs

References ( 4 )
Research paper	Pilgram et al., 2011, J. Neurosci. 31(2): 492--500 The RhoGAP crossveinless-c Interacts with Dystrophin and Is Required for Synaptic Homeostasis at the Drosophila Neuromuscular Junction. [FBrf0212767] Fradkin et al., 2008, J. Neurosci. 28(19): 5105--5114 The dystrophin Dp186 isoform regulates neurotransmitter release at a central synapse in Drosophila. [FBrf0204668] Shcherbata et al., 2007, EMBO J. 26(2): 481--493 Dissecting muscle and neuronal disorders in a Drosophila model of muscular dystrophy. [FBrf0192541] van der Plas et al., 2006, J. Neurosci. 26(1): 333--344 Dystrophin is required for appropriate retrograde control of neurotransmitter release at the Drosophila neuromuscular junction. [FBrf0191057]

Allele Dmel\DysE6

Allele Dmel\Dys^E6