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General Information
Symbol
Dmel\GluRIIAAD9
Species
D. melanogaster
Name
FlyBase ID
FBal0318459
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
dglur-IIAg9, dglurIIAAD9
Key Links
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Comment:

Deletion of entire coding region of GluRIIA, plus 300bp of 5' flanking sequence and a similar extent of 3' flanking sequence. The position of the deletion on the reference sequence is approximate and was inferred by the FlyBase curator based on the author statement.

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Cytology
Nature of the lesion
Statement
Reference

Entire coding region of GluRIIA has been deleted, plus 300bp of 5' flanking sequence and a similar extent of 3' flanking 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 ( 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

GluRIIAAD9 heterozygous third instar larvae display significant deficit in locomotion (measured as distance crawled per unit of time).

In homozygous GluRIIAAD9 mutants all A-type receptors are absent, whereas B-type receptor clusters are still present in the neuromuscular junction.

Latrunculin A treatment of GluRIIAAD9 mutants has no effect on receptor cluster size or sEJC amplitude (compared to a reduction in wild-type). Similarly, postsynaptic latrunculin has no effect on sEJC amplitude in GluRIIAAD9 mutants.

The mean sEJC amplitude in GluRIIAAD9 mutants is approximately one-half the amplitude of wild-type animals, consistent with complete and specific loss of A-type receptors.

The morphological development of neuromuscular junctions (NMJs) in GluRIIAAD9/Df(2L)cl-h4 mutants is indistinguishable from wild type when larvae are reared at 18 or 25oC. However, when wild-type larvae are raised at 29oC, size-matched animals show consistently larger and more complex NMJs with more boutons. This bouton outgrowth does occur in GluRIIAAD9/Df(2L)cl-h4 mutants reared at 29oC, but to a much lower extent than wild type. At 29oC, GluRIIAAD9/Df(2L)cl-h4 mutants show an increase in stride-frequency that is comparable to wild type, but a lower increase in speed of locomotion and crawling distance than that seen in wild type and no change in stride frequency, which does increase in wild type. The mutants have an altered locomotor pattern to wild-type larvae; they rest more and show only short stretches of uninterrupted movement.

GluRIIAAD9/Df(2L)cl-h4 flies have a postsynaptic defect, which causes a reduction in average quantal size and an increased junctional quantal content. At the larval stage, these mutants develop fewer presynaptic boutons but, as compensation, they have a greater density of T-bars within these boutons compared to wild type. This results in the release of more vesicles per action potential and the production of larger evoked Ca2+ signals. However, there is still a strong depression of postsynaptic responses that saturate at around 60% of the initial enhanced excitatory junctional potential (eEJP) amplitude.

Shows no obvious behavioral phenotype. Heterozygotes with Df(2L)cl-h4 show large decrease in quantal size, as recorded in muscle 6, segment A3 of female third instar larvae. There is no change in evoked release, indicating a compensatory increase in number of vesicles released, i.e. in quantal content. This is confirmed by failure analysis, using reduced external calcium concentrations. There is a small but significant decrease in bouton number on muscles 6 and 7 in the mutant. The up-regulation of transmitter release is observed over a range of calcium concentrations. Short-term facilitation is not altered at 10Hz or 20Hz.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Statement
Reference
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference

The elimination of one copy of GluRIIA in pAbpk10109/+, GluRIIAAD9/+ mutants results in an almost complete suppression of enhanced junctional signal transmission and in a corresponding suppression of junctional growth, indicating that animals with genetically restricted GluRIIA expression are incapable of developing a strengthened larval stage neuromuscular junction.

Xenogenetic Interactions
Statement
Reference

Scer\GAL4elav-C155-mediated expression of Avic\GFPCameleon2.0.Scer\UAS does not affect the neurological phenotype of GluRIIAAD9 mutants.

Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
Comments
Comments

Null allele.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (13)
Reported As
Name Synonyms
Secondary FlyBase IDs
  • FBal0085985
  • FBal0160418
References (14)