FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\Nlg2KO70
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General Information
Symbol
Dmel\Nlg2KO70
Species
D. melanogaster
Name
FlyBase ID
FBal0258113
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
dnlg2KO70
Key Links
Allele class
Nature of the Allele
Allele class
Progenitor genotype
Associated Insertion(s)
Cytology
Description

A 2kb fragment of Nlg2 from the start codon to the middle of the first intron has been replaced by a w+mW.hs marker.

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 ( 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

Nlg2KO70 mutant adults do not show adult locomotor activity defects.

Nlg2KO70 homozygous mutant adults do not show any defects in the medulla columnar restriction of the axonal branches of L4 lamina neurons.

The neuromuscular junctions of Nlg2KO70 third instar larvae exhibit a significant decrease in the number of synaptic boutons.

The number of boutons at the neuromuscular junction is significantly reduced compared to wild type in mutant third instar larvae.

Homozygous third instar larval show a reduction in EJP amplitude at the neuromuscular junction compared to controls. mEJP amplitude is not significantly altered. Quantal content is significantly reduced.

Homozygous neuroliginKO70 mutants exhibit no detectable abnormalities in body size or morphology.

Neither the amplitude nor frequency of spontaneously occuring mEJPs are significantly different to wild-type in homozygous neuroliginKO70 and heterozygous neuroliginKO70/Df(2L)ED7007 mutants. In contrast, the amplitude of stimulus-evoked EJPs shows a small but significant increase in neuroliginKO70 and neuroliginKO70/Df(2L)ED7007 mutants. These effects are seen at both high (0.8mM) and low (0.2mM) calcium levels.

neuroliginKO70 mutants exhibit a decrease in paired-pulse plasticity (where pairs of stimuli are given and the ratio between the amplitude generated from each pulse is calculated), indicating an increase in transmitter release probability.

Both the rise time and decay time of stimulus-evoked EJPs are significantly reduced in neuroliginKO70 mutants. These reductions are observed in both 0.8mM and 0.2mM calcium backgrounds.

At a macromolecular level, synapses are formed with a wild-type pattern of innervations in neuroliginKO70 mutants. However, the number of boutons is significantly reduced in these mutants compared to wild-type. The decreased number of boutons is associated with a significant decrease in the extent of synaptic arborization in neuroliginKO70 mutants.

neuroliginKO70 synapses exhibit smaller post-synaptic density zones and increased density of active zones. Individual T-bars appear to be normal in shape, but the total number of these structures per bouton is significantly increased.

neuroliginKO70 mutants exhibit defects in post-synaptic organisation, specifically the reduction in length of post-synaptic density regions and a reduction in thickness of subsynaptic reticulum structures.

In early second-instar larvae, neuroliginKO70 mutants show a significant reduction in bouton numbers compared with wild-type.

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

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

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

Other
Additional Comments
Genetic Interactions
Statement
Reference

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.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

Expression of Nlg2Scer\UAS.cSa postsynaptically, under the control of either Scer\GAL4C57 or Scer\GAL4how-24B, does not rescue the reduction in bouton number seen at the neuromuscular junction in Nlg2KO70 third instar larvae. However, expression of Nlg2Scer\UAS.cSa in both neurons and muscles, under the control of Scer\GAL4αTub84B.PL, restores bouton number at the neuromuscular junction in Nlg2KO70 third instar larvae to wild-type levels.

Expression of Nlg2Scer\UAS.cSa under the control of either Scer\GAL4how-24B or Scer\GAL4elav.PU does not rescue the reduced EJP amplitude seen at the neuromuscular junction in Nlg2KO70 third instar larvae. Expression under the control of Scer\GAL4αTub84B.PL rescues the EJP amplitude to wild type.

The increase in the number of T-bars seen per bouton in neuroliginKO70 mutants is rescued upon expression of neuroliginScer\UAS.cSa by Scer\GAL4how-24B.

Defects in post-synaptic organisation, specifically in the length of post-synaptic density regions and the thickness of subsynaptic reticulum structures are rescued upon expression of neuroliginScer\UAS.cSa post-synaptically under the control of Scer\GAL4C57.

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External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
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Name Synonyms
Secondary FlyBase IDs
    References (8)