FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\Nrgl7
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General Information
Symbol
Dmel\Nrgl7
Species
D. melanogaster
Name
FlyBase ID
FBal0013172
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
Nrg17, nrg2, l(1)VA142
Key Links
Genomic Maps

Nature of the Allele
Progenitor genotype
Cytology
Description

Amino acid replacement: W80term.

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Nucleotide change:

G8544885A

Amino acid change:

W80term | Nrg-PA; W80term | Nrg-PB; W80term | Nrg-PC; W80term | Nrg-PD; W80term | Nrg-PE; W80term | Nrg-PF; W80term | Nrg-PG; W80term | Nrg-PH; W80term | Nrg-PI

Reported amino acid change:

W80term

Comment:

G to A nucleotide change at the second or third position of the Trp codon leads to a nonsense mutation (exact site of mutation unspecified). Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid chang

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 ( 1 )
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

Nrgl7/Nrgl7 embryos display a synaptic defect similar to that seen in mir-8Δ/mir-8Δ (ISNb motor axons innervation defect at m6/7), though with reduced penetrance.

The olfactory receptor neurons of Nrgl7 mutant flies do not show any overt phenotype, either in uninjured flies or in flies in which the antennae have been surgically ablated.

56% of dorsal da neuron E (ddaE) and 14% of ddaD neurons show ectopic branches on their axons at 19-20 hours after egg laying (AEL) in Nrgl7 embryos. In addition, the dendritic arbors of ddaD and ddaE are deformed and this phenotype can be detected at 18-19 hours AEL.

Embryos that express NrgScer\UAS.T:Ivir\HA1, under the control of Scer\GAL4IG1-1, in a Nrgl7 background and Scer\GAL4repo show deformed ddaE dendritic arbors.

56% of dorsal da neuron E (ddaE) and 14% of ddaD neurons show ectopic branches on their axons in Nrgl3 embryos. The dendritic branches of ddaD cover a smaller field and have fewer terminals than wild-type ddaD neurons.

Nrgl10/Nrgl7 females are viable at 18[o]C but are inviable at 25[o]C.

Nrg849/Nrgl7 and Nrg892/Nrgl7 females show normal sexual receptivity when mated to wild-type males.

In Nrgl7 homozygous embryos, tracheal phenotypes are apparent from stage 15. At stage 16 in these embryos the average dorsal trunk length is significantly greater than wild type (P<0.005) (121+/-2% mean+/-s.e.m., n>5, normalized to stage 16 wild-type value). In addition these embryos have moderately severe diameter increases in the dorsal trunk and other primary tracheal branches, and some ganglionic branches exhibit missing lumen. Unlike wild-type, post stage 15 trachea in Nrgl7 homozygotes are unable to exclude from their lumens, a fluorescently labelled 10kDa dextran injected into the body cavity. This is consistent with these trachea lacking a functioning septate junction barrier.

Homozygous embryos show a general disorganisation of the peripheral nervous system cell bodies. The aCC and SNb motoneurons often show a stalled phenotype, failing to extend normally, and SNb motoneurons sometimes show abnormal contacts with their targets.

Nrgl7 is lethal during the late embryonic and early larval phase of development. It has no maternal effect component.

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

Nrgl7 is an enhancer of phenotype of Nrt5

Nrgl7 is an enhancer of axon | embryonic stage phenotype of Nrt1

Additional Comments
Genetic Interactions
Statement
Reference

Removing one copy of eve in Nrgl7/Y mutants results in more severe intersegmental nerve guidance defects with a significant increase in axon stalling upon the addition of eveΔRP2A.

Nrgl7 dominantly enhances the shortening of dendritic length and the reduction in the number of dendritic endpoints of dorsal dendritic arborisation neurons which is seen in larvae expressing NakdsRNA.Scer\UAS under the control of Scer\GAL4elav-C155.

Increases the frequency of Fas2 expressing axons showing defects in Nrt1/Nrt5, Nrt1/Nrt1 and Nrt5/Nrt5 embryos.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Partially rescued by
Not rescued by
Comments

Expression of Nrg+t25 fully rescues Nrgl7 mutant embryonic lethality.

Expression of Nrg167ΔFIGQY fully rescues Nrgl7 mutant embryonic lethality.

Expression of Nrg180ΔFIGQY fully rescues Nrgl7 mutant embryonic lethality.

Expression of NrgΔIg3-4 fails to rescue Nrgl7 mutant embryonic lethality.

The reduced female receptivity phenotype of Nrgibx is complemented by Nrgl7.

Nrgl7 complements the reduced female receptivity phenotype of Nrg892.

Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer

Lefevre.

Comments
Comments

Complements: ibxM72.

Maternal germline clonal analysis demonstrates there is no maternal effect.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (10)
References (24)