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General Information
Symbol
Dmel\JraJbz.UAS
Species
D. melanogaster
Name
FlyBase ID
FBal0215807
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-junDN, UAS-Jbz
Nature of the Allele
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

UASt regulatory sequences drive expression of amino acids 183-289 (the bZIP region) of Jra.

UASt regulatory sequences drive expression of the basic region and leucine zipper (amino acids 183-289) of Jra.

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 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Expressing JraJbz.UAS under the control of Scer\GAL4tey-5053A (together with Dicer-2, for efficient RNAI) does not provide protection against (injury-induced) Wallerian degeneration of third instar larval motoneurons.

Overexpression of JraJbz.Scer\UAS in combination with Scer\GAL4Scer\UAS.cHa driven by Scer\GAL4Tab2-201Y does not affect axon pruning.

Expression of JraJbz.Scer\UAS under the control of Scer\GAL4D42 in the presence of Scer\GAL80Cha.PK (to suppress expression in cholinergic neurons) results in a significant decrease in total dendritic length and in the number of dendritic branches in MN5 motorneurons.

Expression of JraJbz.Scer\UAS using Scer\GAL4ey-OK107 does not result in any gross axonal phenotypes.

Expression of JraJbz.Scer\UAS in the RP2 motor neurons (using the Scer\GAL4eve.RRK driver to drive expression of Scer\FLP1Scer\UAS.cUa which then induces clones of cells expressing Scer\GAL4Act.PU) results in a significant decrease in RP2 dendrite volume compared to controls.

Expression of JraJbz.Scer\UAS under the control of Scer\GAL4elav.PH in clones induced by FLP/FRT mediated recombination (to activate the Scer\GAL4elav.PH driver) results in a decrease in the number of type 1b boutons at muscle 13 compared to wild type.

Expression of JraJbz.Scer\UAS under the control of Scer\GAL4elav-C155 results in an approximately 25% reduction in EJC amplitude (synaptic strength) and bouton number at the larval neuromuscular junction. mEJC amplitude is not significantly altered.

Scer\GAL4-mediated expression in the eye imaginal disc interferes with proper eye development.

Causes no effect on copper cell development, when expression is driven by Scer\GAL448Y.

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

rawdcp-1 homozygotes show protection against (injury-induced) Wallerian degeneration in third instar larval motor neurons, which is considerably suppressed by the expression of JraJbz.UAS under the control of Scer\GAL4tey-5053A; in these double mutants, injured axons exhibit severely decreased new growth/sprouting compared to controls.

The synaptic overgrowth phenotype (increase in bouton number) seen at the neuromuscular junction in larvae derived from homozygous SkpAGD65 females is partially suppressed by expression of JraJbz.Scer\UAS under the control of Scer\GAL4elav.PU.

The reduction in total dendritic length and in the number of dendritic branches which is seen in MN5 motorneurons in animals expressing JraJbz.Scer\UAS under the control of Scer\GAL4D42 in the presence of Scer\GAL80Cha.PK (to suppress expression in cholinergic neurons) is not altered if the flies are also simultaneously co-expressing both ShDN.EKI.Scer\UAS and eagDN.EKI.Scer\UAS.

Co-expression of kayFbz.Scer\UAS and JraJbz.Scer\UAS results in axon degeneration phenotypes.

Co-expression of two copies of JraJbz.Scer\UAS strongly enhances the axonal defects seen in Scer\GAL4ey-OK107, bskGD10555 animals.

The border follicle cell migration defects that are seen in flies co-expressing both PvrDN.Scer\UAS and hepAct.Scer\UAS under the control of Scer\GAL4slbo.2.6 are not strongly affected by the co-expression of JraJbz.Scer\UAS.

Expression of JraJbz.Scer\UAS, under the control of Scer\GAL4BG380 does not suppress the hiwND8 synaptic phenotype.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
Comments
Comments

Protein acts as a dominant negative as the bZIP domain is able to dimerize and bind DNA without being able to stimulate transcription.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (5)
Reported As
Symbol Synonym
JraJbz.Scer\UAS
JraJbz.UAS
JrabZIP.Scer\UAS
JrabZIP.UAS
Name Synonyms
Secondary FlyBase IDs
  • FBal0060635
  • FBal0063160
References (20)