Allele Dmel\Dys^{dsRNA.NH2.Scer\UAS}

General Information
Symbol	Dmel\Dys^{dsRNA.NH2.Scer\UAS}	Species	D. melanogaster
Name		FlyBase ID	FBal0216503
Feature type	allele	Associated gene	Dmel\Dys

Allele class
Mutagen	in vitro construct - regulatory fusion, in vitro construct - RNAi
Recent Updates
Description	What does this section display? This section contains items that were added to this record for each release. It currently only tracks new links between this FlyBase report and other FlyBase data classes (e.g. genes, references, stocks) or controlled vocabulary terms (e.g. GO, anatomy terms). What does this section not display? This section does not currently display links that were removed or gene model changes.
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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	in vitro construct - regulatory fusion (van der Plas et al., 2006) in vitro construct - RNAi (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
Nature of the lesion	Statement Reference Scer\UAS regulatory sequences drive expression of Dys coding sequences specific to the large isoform of Dys (base pairs 610-1532) which are separated by an 816bp spacer fragment (which is derived from an intron of mub). (van der Plas et al., 2006)
Cytology
Phenotypic Data
Phenotypic Class
	neurophysiology defective, with Scer\GAL4^G14 (van der Plas et al., 2006) neurophysiology defective, with Scer\GAL4^how-24B (van der Plas et al., 2006)
Phenotype Manifest In

Detailed Description
	Statement Reference Expression of Dys^{dsRNA.NH2.Scer\UAS} in the muscle, under the control of either Scer\GAL4^how-24B or Scer\GAL4^G14 results in quantal content levels that are increased to levels similar to that seen in Dys mutants (i.e. approximately 70% higher than controls). Expression of Dys^{dsRNA.NH2.Scer\UAS} pre-synaptically, under the control of Scer\GAL4^elav-C155 does not change quantal content levels compared to wild-type larvae. (van der Plas et al., 2006)
External Data
Linkouts
Interactions
Phenotypic Class
NOT Enhancer of
Statement Reference Scer\GAL4^G14/Dys^{dsRNA.NH2.Scer\UAS} is a non-enhancer of neurophysiology defective phenotype of wit^B11/wit^A12 (van der Plas et al., 2006)
NOT Suppressor of
Statement Reference Scer\GAL4^G14/Dys^{dsRNA.NH2.Scer\UAS} is a non-suppressor of neurophysiology defective phenotype of wit^B11/wit^A12 (van der Plas et al., 2006)
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement Reference Expression of Dys^{dsRNA.NH2.Scer\UAS} postsynaptically (under the control of Scer\GAL4^G14) in wit^A12/wit^B11 trans-heterozygous neuromuscular junctions results in similar EJP amplitudes and quantal content as in wit^A12/wit^B11 mutants. (van der Plas 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 ( 2 )
Reported As
Symbol Synonym	det^{dsRNA.NH2.Scer\UAS} Dys^{dsRNA.NH2.Scer\UAS}
Name Synonym
Secondary FlyBase IDs

References ( 1 )
Research paper	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\DysdsRNA.NH2.Scer\UAS

Allele Dmel\Dys^{dsRNA.NH2.Scer\UAS}