FB2024_03 , released June 25, 2024
Allele: Dmel\Nrg180.I.UAS
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General Information
Symbol
Dmel\Nrg180.I.UAS
Species
D. melanogaster
Name
FlyBase ID
FBal0147728
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-nrg180, UAS-nrg, UAS-nrg180, UAS-NRG-180
Key Links
Transgenic product class
Nature of the Allele
Transgenic product class
Progenitor genotype
Carried in construct
Cytology
Description

The MtnA promoter is replaced with UASt sequences.

Allele components
Component
Use(s)
Encoded product / tool
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
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 ( 1 )
Disease
Interaction
References
ameliorates  epilepsy
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Embryos with Nrg180.I.Scer\UAS driven by Scer\GAL4elav.PU do not have intersegmental nerve branch ISNb motor axon innervation defects; when driven by Scer\GAL4how-24B, there is an ISNb axon arrest phenotype.

Expression of Nrg180.I.Scer\UAS in a Df(2R)eve mutant background, under the control of Scer\GAL4eve.RN2 leads to both aCC and RP2 motor neurons displaying an almost exclusively single exit from the CNS.

The number of dendritic endpoints of dorsal dendritic arborisation neurons is reduced compared to controls in larvae expressing Nrg180.I.Scer\UAS under the control of Scer\GAL4elav-C155.

When Nrg180.I.Scer\UAS is driven by Scer\GAL4GMR.PF no effects are seen on the number of photoreceptor cells or cone cells present in the eye.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Enhancer of
Suppressor of
Other
Phenotype Manifest In
Enhanced by
Enhancer of
Statement
Reference
Suppressor of
Other
Additional Comments
Genetic Interactions
Statement
Reference

Expression of Nrg180.I.Scer\UAS driven by Scer\GAL4elav.PU significantly partially suppresses the intersegmental nerve branch ISNb motor axon innervation defects (of m6/7) seen in mir-8Δ/mir-8Δ embryos. Expression of Nrg180.I.Scer\UAS driven by Scer\GAL4how-24B significantly partially (only 10%) suppresses the intersegmental nerve branch ISNb motor axon innervation defects (of m6/7) seen in mir-8Δ/mir-8Δ embryos.

Expression of Nrg180.I.Scer\UAS in an eveΔRP2A mutant background results in the exit of a single motoneuron of the pair in each hemisegment.

Co-expression of beat-IaScer\UAS.cFa and Nrg180.I.Scer\UAS in a Df(2R)eve mutant background, under the control of Scer\GAL4eve.RN2 leads to a more robust CNS exit for motor neurons, with many hemisegments displaying exit of both motor neurons. There are two types of exit: unfasciculated, both axons from the same hemisegment chose a different nerve root, or fasciculated, where axons join and exit through the intersegmental nerve root.

Co-expression of unc-5Scer\UAS.T:Ivir\HA1,T:SS-wg and Nrg180.I.Scer\UAS in a Df(2R)eve mutant background, under the control of Scer\GAL4eve.RN2 leads to a more robust CNS exit for motor neurons, with many hemisegments displaying exit of both motor neurons. There are two types of exit: unfasciculated, both axons from the same hemisegment chose a different nerve root, or fasciculated, where axons join and exit through the intersegmental nerve root.

Co-expression of unc-5Scer\UAS.T:Ivir\HA1,T:SS-wg, beat-IaScer\UAS.cFa and Nrg180.I.Scer\UAS in a Df(2R)eve mutant background, under the control of Scer\GAL4eve.RN2 leads to a more robust CNS exit for motor neurons, with many hemisegments displaying exit of both motor neurons. The number of hemisegments with one neuronal exit is reduced, compared to controls and single and double mutants.

Combinatorial misexpression of unc-5Scer\UAS.T:Ivir\HA1,T:SS-wg with Nrg180.I.Scer\UAS under the control of Scer\GAL4eg-Mz360, results in lateral exit of 8% of EW axons.

Triple misexpression of unc-5Scer\UAS.T:Ivir\HA1,T:SS-wg, beat-IaScer\UAS.cFa, and Nrg180.I.Scer\UAS in EW neurons, under the control of Scer\GAL4eg-Mz360, leads to lateral redirection of axons in 20% of hemisegments.

Quadrupal misexpression of unc-5Scer\UAS.T:Ivir\HA1,T:SS-wg, beat-IaScer\UAS.cFa, Nrg180.I.Scer\UAS and Fas2Scer\UAS.cLa in EW neurons, under the control of Scer\GAL4eg-Mz360, leads to lateral redirection of axons in 33% of hemisegments.

The addition of Nrg180.I.Scer\UAS enhances the rough eye phenotype seen in edScer\UAS.cBa, Scer\GAL4GMR.PF animals with a reduction in the number of ommatidia and a decrease in the number of bristles. In addition, a significantly higher percentage of ommatidia contain fewer photoreceptor and cone cells.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

Expression of Nrg180.I.Scer\UAS under the control of either Scer\GAL4Mef2.247, Scer\GAL430Y, Scer\GAL4Tab2-201Y or Scer\GAL4c316 does not result in any clear evidence of rescue the Nrgibx central brain phenotype.

Expression of Nrg180.I.Scer\UAS under the control of either Scer\GAL4Mef2.247, Scer\GAL430Y or Scer\GAL4c316 results in a small but significant increase in the sexual receptivity of Nrgibx females, while expression under the control of Scer\GAL4Tab2-201Y has no significant effect.

Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
Reported As
Symbol Synonym
Nrg180.I.Scer\UAS
Nrg180.I.UAS
Name Synonyms
Secondary FlyBase IDs
    References (12)