FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\Nrx-1Δ83
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General Information
Symbol
Dmel\Nrx-1Δ83
Species
D. melanogaster
Name
FlyBase ID
FBal0258010
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
dnrx83, dnrxΔ83, nrxΔ83
Key Links
Genomic Maps

Allele class
Nature of the Allele
Allele class
Progenitor genotype
Cytology
Description

Mobilisation of P{XP}Nrx-1d08766 by Δ2-3 transposase results in a 4066bp deletion.

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

Reported as a 4066 bp deletion resulting from the imprecise excsion of P{XP}Nrx-1d08766 extending from tgccgagtaacaccaacac to tatctcccatttctcatgac.

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 ( 1 )
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

Unlike in wild-type, the axon of L4 lamina neuron in Nrx-1Δ83 homozygous as well as Nrx-1Δ83/Nrx-1273 transheterozygous adults is not restricted to a single medulla column but often extends to neighboring columns, although the axons still terminate appropriately in the M4 layers.

Third instar neuromuscular junctions of Nrx-1273/Nrx-1Δ83 mutants exhibit a significant Ca[2+]-concentration-dependent reduction in excitatory junction current (EJC) amplitude, and a small but significant reduction in steady-state quantal content, in response to a 1-Hz train of stimulation, as compared to wild type. In response to 40 Hz tetanic nerve stimulation, NMJs in these mutants show a marked activity-dependent reduction in the amplitude of EJCs under 0.5mM Ca[2+] conditions, show rapid synaptic depression with amplitude of evoked currents showing a steeper decline after 8 stimuli under 1.8mM Ca[2+] conditions, and show a significant reduction in steady state EJC and quantal content, but no significant difference in steady state miniature EJC (mEJC), as compared to wild type.

Mutant flies show a reduced phototactic response to light compared to wild type. Mutant photoreceptors show approximately 10,000-fold light sensitivity compared to wild type. Mutant flies do not show a blue light-induced prolonged depolarization afterpotential.

Mutant photoreceptors have a normal endoplasmic reticulum structure at 65% of pupal development. However, at 79% of pupal development, the endoplasmic reticulum appears expanded.

neuroanatomy defective, enhanceable { neuroligin[KO70]/+ }

Nrx-1Δ83 larvae display a severe defect in locomotion and a 49% decrease in bouton number at neuromuscular junctions.

Nrx-1Δ83 neuromuscular junctions show a severe reduction in synaptic vesicle trafficking.

Nrx-1Δ83/+ neuromuscular junctions show a small but significant reduction in synaptic vesicle trafficking.

Induced excitatory potential (EJP) amplitude at Nrx-1Δ83 neuromuscular junctions is significantly decreased compared to wild type.

Nrx-1Δ83/+ neuromuscular junctions show a small but significant reduction in EJP amplitude.

Both the spontaneous miniature excitatory potential (mEJP) amplitude and frequency at Nrx-1Δ83 neuromuscular junctions are significantly increased compared to wild type.

Nrx-1Δ83 and Nrx-1Δ83/Df(3R)Exel6191 mutants are viable and fertile, with no obvious developmental defects.

Nrx-1Δ83 mutants are short-lived. At 37 days, only 32.5% of Nrx-1Δ83 mutants are alive, compared with 82.5% of wild-type and 79% of rescue flies (Scer\GAL4elav-C155/+; Nrx-1Scer\UAS.cZa/+; Nrx-1Δ83).

Nrx-1Δ83 and Nrx-1Δ83/Df(3R)Exel6191 mutants exhibit fewer synapses than controls (approximately half).

Associative learning is reduced in Nrx-1Δ83 mutants (testing for their ability to associate odors with a fructose reward in an individual-animal assay).

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference
NOT Enhanced by
Statement
Reference
Enhancer of
Statement
Reference
NOT Enhancer of
Other
Phenotype Manifest In
Enhanced by
Statement
Reference

Nrx-1Δ83 has bouton | second instar larval stage phenotype, enhanceable by neuroligin[+]/Nlg2KO70

Nrx-1Δ83 has synapse | second instar larval stage phenotype, enhanceable by neuroligin[+]/Nlg2KO70

Nrx-1Δ83 has synaptic vesicle phenotype, enhanceable by CASKX-307/CASK[+]

NOT Enhanced by
Statement
Reference

Nrx-1Δ83 has axon | adult stage phenotype, non-enhanceable by Nlg4KO10/Nlg4KO10

Nrx-1Δ83 has medulla | adult stage phenotype, non-enhanceable by Nlg4KO10/Nlg4KO10

Enhancer of
Statement
Reference

Nrx-1[+]/Nrx-1Δ83 is an enhancer of bouton | second instar larval stage phenotype of Nlg2KO70

Nrx-1[+]/Nrx-1Δ83 is an enhancer of synapse | second instar larval stage phenotype of Nlg2KO70

Nrx-1[+]/Nrx-1Δ83 is an enhancer of synaptic vesicle phenotype of CASKX-307

NOT Enhancer of
Additional Comments
Genetic Interactions
Statement
Reference

The impaired columnar restriction of L4 lamina neuron axons (which frequently invade adjacent medulla columns) observed in adult flies expressing EphrinHMS01289 under the control of Scer\GAL4GMR31C06 is not worsened further by combination with Nrx-1Δ83/Nrx-1273 (which on its own also causes defects in columnar restriction of the L4 axons).

The frequency of L4 lamina neuron axons aberrantly invading adjacent medulla columns in adult Nlg4KO10,Nrx-1Δ83 double mutants is not significantly different from each of the single mutants.

Homozygous neuroliginKO70;Nrx-1Δ83 double mutants die during the second instar larval stage.

In early second-instar larvae, neuroliginKO70;Nrx-1Δ83 double mutants show a significant reduction in bouton numbers compared with wild-type as in neuroliginKO70 single mutants. However, the double mutants appear to demonstrate more severe synaptic morphology defects than in the single mutants. Consistent with this, neuroliginKO70;Nrx-1Δ83 double mutants show more severe defects in locomotion than either single mutant.

Flies homozygous for neuroliginKO70 and heterozygous for Nrx-1Δ83 are viable and show more severe defects in neuromuscular morphology at both muscles 6/7 and muscle 4 than neuroliginKO70 single mutants.

Nrx-1Δ83 homozygous mutants in a neuroliginKO70 heterozygous background exhibit more severe defects in neuromuscular morphology at both muscles 6/7 and muscle 4 than Nrx-1Δ83 single mutants.

In contrast to either heterozygote alone, Nrx-1Δ83/+, CASKX-307/+ larvae display a marked defect in locomotion.

Similar to either heterozygote alone, Nrx-1Δ83/+, CASKX-307/+ larvae display no significant differences in bouton number at neuromuscular junctions compared to wild type.

Nrx-1Δ83/+, CASKX-307/+ neuromuscular junctions show a much more severe reduction in synaptic vesicle trafficking compared to either single heterozygote.

Nrx-1Δ83/+, CASKX-307/+ neuromuscular junctions show a more severe reduction in induced excitatory potential (EJP) amplitude compared to either single heterozygote.

In contrast to either heterozygote alone, Nrx-1Δ83/+, CASKX-307/+ neuromuscular junctions show a significant increase in the spontaneous miniature excitatory potential (mEJP) amplitude and frequency compared to wild type.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

The defective columnar restriction of L4 lamina neuron axons (which frequently invade adjacent medulla columns) observed in Nrx-1Δ83 mutant adults is fully rescued by expression of Nrx-1Scer\UAS.cZa driven by Scer\GAL4GMR31C06 (but not Scer\GAL4c739). The impaired columnar restriction is also largely restored by Scer\GAL4GMR31C06-controlled expression that is restricted to 48-60 hr after puparium formation (APF) time window using tub-Gal80[ts], while expression induced between 80-92 hr APF fails to rescue the defect.

Expression of Nrx-1Δ1760-1813.Scer\UAS driven by Scer\GAL4GMR31C06 however cannot rescue the L4 axonal targeting defects of Nrx-1Δ83 mutants.

Expression of Nrx-1Scer\UAS.cZa (but not Nrx-1ΔPBD.Scer\UAS or Nrx-1ΔC.Scer\UAS) under the control of Scer\GAL4RapGAP1-OK6 rescues the rapid synaptic depression seen in third instar Nrx-1273/Nrx-1Δ83 mutant NMJs under 1.8mM Ca[2+] conditions, and expression of Nrx-1Scer\UAS.cZa or Nrx-1ΔPBD.Scer\UAS (but not Nrx-1ΔC.Scer\UAS) rescues the reduced mean EJCs, and the reduced quantal content at the steady state seen in third instar Nrx-1273/Nrx-1Δ83 mutant NMJs under 1.8mM Ca[2+] conditions.

Expression of Nrx-1ΔPBD.Scer\UAS or Nrx-1Scer\UAS.cZa under the control of Scer\GAL4RapGAP1-OK6 restores the decreased initial EJC amplitude and the reduced mean EJCs at the steady state observed in third instar Nrx-1273/Nrx-1Δ83 mutant NMJs under 0.5mM Ca[2+] conditions.

Expression of Nrx-1ΔPBD.Scer\UAS under the control of Scer\GAL4RapGAP1-OK6 restores the decreased initial EJC amplitude but not the the reduced mean EJCs at the steady state observed in third instar Nrx-1273/Nrx-1Δ83 mutant NMJs under 0.5mM Ca[2+] conditions.

The reduced light sensitivity of Nrx-1Δ83 photoreceptors is rescued by expression of Nrx-1Scer\UAS.cTa under the control of Scer\GAL4GMR.PU.

Synapse number is rescued in Scer\GAL4elav-C155/+; Nrx-1Scer\UAS.cZa/+; Nrx-1Δ83 flies.

Longevity is rescued in Scer\GAL4elav-C155/+; Nrx-1Scer\UAS.cZa/+; Nrx-1Δ83 flies.

Associative learning is rescued inScer\GAL4elav-C155/+; Nrx-1Scer\UAS.cZa/+; Nrx-1Δ83 flies.

Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (6)
References (15)