Open Close
General Information
D. melanogaster
FlyBase ID
Feature type
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
Key Links
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
Additional Notes
Associated Sequence Data
DNA sequence
Protein sequence
Progenitor genotype
Carried in construct
Nature of the lesion

UAS sequences drive expression of an artificial, glycosyl phosphatidylinositol (GPI)-anchored form of Nrg.

Allele components
Product class / Tool use(s)
Encoded product / tool
Expression Data
Reporter Expression
Additional Information
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Modifiers Based on Experimental Evidence ( 0 )
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
Disease-implicated variant(s)
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description

Expression of NrgGPI.Scer\UAS pre-synaptically, under the control of Scer\GAL4c17 does not rescue the physiological Nrg849 mutant phenotype.

Expression of NrgGPI.Scer\UAS post-synaptically, under the control of Scer\GAL4shakB.lethal.4.1 does not rescue the physiological Nrg849 mutant phenotype.

Expression of NrgGPI.Scer\UAS pre- and post-synaptically, under the control of Scer\GAL4A307 does not rescue the physiological Nrg849 mutant phenotype.

Overexpression of NrgGPI.Scer\UAS in a wild-type background, either pre- or post-synaptically (under the control of Scer\GAL4c17 or Scer\GAL4shakB.lethal.4.1 respectively) has a mildly disruptive effect on synapse function and morphology, but is synergistically enhanced by simultaneous expression on both sides of the synapse (under the control of Scer\GAL4A307).

Expression of NrgGPI.Scer\UAS in the giant fiber system throughout development (under the control of Scer\GAL4A307) mimics the Nrg849 phenotypes; although essentially all giant fiber-tergo-trochanteral motor neuron (GF-TTMn) connections are physiologically disrupted, ~21% of the GF terminals appear to be anatomically normal at the light-microscopic level, whereas ~45% have thin synaptic terminals. A failure to extend a presynaptic terminal laterally in the second thoracic neuromere occurs in ~31% of the cases. Pathfinding defects in the brain are only rarely observed. Trans-synaptic fills between the GF and the TTMn are seen with less penetrance (only ~15% of the dye-injected GFs) compared to wild-type. Although the overall dendritic structure of TTMn is not affected by the expression of NrgGPI.Scer\UAS, large vesicles are occasionally observed in the medial TTMn dendrite.

Expression of NrgGPI.Scer\UAS through Scer\GAL4A307 using the TARGET system during pathfinding has no effect on the giant synapse physiology in adults. The same treatment in a stabilized, mature synapse has only a mild effect on synapse function (eliciting 70%-80% wild-type responses). However, the presence of NrgGPI.Scer\UAS during nascent synapse formation elicits 30%-50% of the wild-type response, and during synapse formation elicits 25% of the wild-type response, while severely disrupting the GF-TTMn connection.

Pre- and postsynaptic expression of NrgGPI.Scer\UAS in the giant fiber system, under the control of Scer\GAL4A307 results in the giant fibers either failing to increase their diameter, or to extend their presynaptic terminals laterally. While the gross anatomy of the tergo-trochanteral motor neuron (TTMn) is unaffected in NrgGPI.Scer\UAS (Scer\GAL4A307) mutants, in about one-third of the preparations, abnormal large vesicles are observed in the medial dendrite.

Targeted expression of NrgGPI.Scer\UAS under the control of Scer\GAL4Bx-MS1096 induces a number of axon guidance defects. Axons from the wing margin sensilla can also tangle and perforate the epithelial surface. At early stages of sensory axon extension, numerous ectopic contacts between axon and epithelium are seen.

Overexpression of NrgGPI.Scer\UAS in wing sensory neurons and two wing epithelial layers, mediated by Scer\GAL4MS1075, causes a reduction in wing size and the appearance of ectopic sensory neurons. Additionally, there are severe axonal pathfinding defects including the distal extension of L1 axons, the absence of the proximal projection where the L1 and L3 nerve join in wild type, the clumping together of L1 axons and the penetration of the wing epithelium by the L1 nerve, an aberrant process which can extend beyond the wing tissue. Expression of NrgGPI.Scer\UAS under Scer\GAL4MS1075 in a Nrgl3 background results in the same phenotype.

External Data
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Suppressed by

NrgGPI.UAS, Nrgl3, Scer\GAL4MS1075 has wing phenotype, suppressible by Egfr[+]/Egfrt1

NrgGPI.UAS, Scer\GAL4MS1075 has wing phenotype, suppressible by Egfr[+]/Egfrt1

NrgGPI.UAS, Scer\GAL4MS1075 has wing phenotype, suppressible by Egfrt1

Additional Comments
Genetic Interactions

The defective wing phenotype of NrgGPI.Scer\UAS; Scer\GAL4MS1075 mutants is partially suppressed in a Egfrt1 or Egfrt1/+ background. Egfrt1 also suppresses the wing phenotype when NrgGPI.Scer\UAS is expressed in a Nrgl3 background.

Xenogenetic Interactions
Complementation and Rescue Data
Images (0)
Stocks (1)
Notes on Origin
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
Reported As
Symbol Synonym
Name Synonyms
Secondary FlyBase IDs
    References (6)