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General Information
Symbol
Dmel\nosdsRNA.UAS.WIZ
Species
D. melanogaster
Name
FlyBase ID
FBal0322536
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-nosRNAi
Key Links
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Carried in construct
Cytology
Nature of the lesion
Statement
Reference

UAS regulatory sequences drive expression of an inverted repeat of nos sequence (nucleotides 744-1203 in exon 2). The repeats are in tail-to-tail orientation and are separated by a w intron.

Allele components
Product class / Tool use(s)
Encoded product / tool
Expression Data
Reporter Expression
Additional Information
Statement
Reference
 
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Expression of nosdsRNA.Scer\UAS.WIZ RNAi under the control of Scer\GAL4477 results in dendritic field coverage defects and loss of terminal branches in class IV dendritic arborizing (da) neurons in third instar larvae due to net loss rather than gain of terminal branches during mid-to-late third larval instar. nosdsRNA.Scer\UAS.WIZ RNAi expressing neurons display perturbed branch dynamics as the retraction rates are highly increased. Expression under the Scer\GAL4ppk.1.9 driver leads to a significantly increased density of mitochondria in dendrites compared to controls.

Expression of nosdsRNA.Scer\UAS.WIZ driven by Scer\GAL4elav-C155 or Scer\GAL4how-24B results in a significant increase in total bouton number at the third instar larval neuromuscular junction, compared to controls; the number of active zones in type 1s boutons is significantly increased with expression driven by Scer\GAL4elav-C155. Expression of nosdsRNA.Scer\UAS.WIZ driven by Scer\GAL4Mhc.PU results in a significant decrease in GluRIIA (and increase in GluRIIB) immunoreactivity at NMJ boutons. Recordings from the NMJ of Scer\GAL4Mhc.PU>nosdsRNA.Scer\UAS.WIZ larvae show a significant decrease in mEJP (mini) amplitude and faster mEJP decay times, compared to controls.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Suppressed by
Statement
Reference
NOT suppressed by
Additional Comments
Genetic Interactions
Statement
Reference

The dendritic field coverage defects and loss of terminal branches observed in class IV dendritic arborizing neurons of third instar larvae expressing nosdsRNA.Scer\UAS.WIZ under the control of Scer\GAL4477 is suppressed by combination with a single copy of hidA206 or Df(3L)H99 or by co-expression of hidGD1673 RNAi or Diap1Scer\UAS.cHa but not by combination with both Df(3L)grimC15E and rpr87 (one copy each). The increased branch retraction rate characteristic for nosdsRNA.Scer\UAS.WIZ RNAi (driven by Scer\GAL4477) expressing larvae as well as the increased density of mitochondria in dendrites (RNAi driven by Scer\GAL4ppk.1.9) are also rescued by combination with hidA206.

Xenogenetic Interactions
Statement
Reference

The dendritic field coverage defects and loss of terminal branches observed in class IV dendritic arborizing neurons of third instar larvae expressing nosdsRNA.Scer\UAS.WIZ under the control of Scer\GAL4477 is suppressed by co-expression of BacA\p35Scer\UAS.cUa.

Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
Reported As
Symbol Synonym
nosdsRNA.Scer\UAS.WIZ
nosdsRNA.UAS.WIZ
Name Synonyms
Secondary FlyBase IDs
    References (3)