Allele Dmel\GluRIIA^AD9

General Information
Symbol	Dmel\GluRIIA^AD9	Species	D. melanogaster
Name		FlyBase ID	FBal0085985
Feature type	allele	Associated gene	Dmel\GluRIIA
Also Known As	dglurIIA^AD9

Map ( GBrowse )
Allele class	loss of function allele
Mutagen	P-element activity
Recent Updates
Description	What does this section display? This section contains items that were added to this record for each release. It currently only tracks new links between this FlyBase report and other FlyBase data classes (e.g. genes, references, stocks) or controlled vocabulary terms (e.g. GO, anatomy terms). What does this section not display? This section does not currently display links that were removed or gene model changes.
Update Feed	Click the icon below to subscribe to this FlyBase record and receive updates automatically through your feed reader.
FB2013_03
FB2013_02
All updates	Click here to see a list of all updates to this record from FB2010_08 and on.
Nature of the Allele
Allele class	loss of function allele (Petersen et al., 1997)
Mutagen	P-element activity (Petersen et al., 1997)
Mutations Mapped to the Genome

Type Location Additional Notes References sequence variant 2L:5,555,004..5,558,997 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. evidence=experimental (Petersen et al., 1997)
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype	P{lacW}72 (Petersen et al., 1997) P{lacW}228 (Petersen et al., 1997)
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. (Petersen et al., 1997)
Cytology
Phenotypic Data
Phenotypic Class
	locomotor behavior defective \| heat sensitive (with Df(2L)cl-h4) (Sigrist et al., 2003) neuroanatomy defective (Petersen et al., 1997, Chen et al., 2005) neuroanatomy defective (with Df(2L)cl-h4) (Reiff et al., 2002) neurophysiology defective (Chen et al., 2005) neurophysiology defective (with Df(2L)cl-h4) (Reiff et al., 2002) viable (Petersen et al., 1997, DiAntonio et al., 1999)
Phenotype Manifest In
	bouton (Petersen et al., 1997) embryonic/larval neuromuscular junction \| heat sensitive (with Df(2L)cl-h4) (Sigrist et al., 2003) synapse (Petersen et al., 1997) synaptic vesicle (Petersen et al., 1997) t-bar (with Df(2L)cl-h4) (Reiff et al., 2002) type I bouton (with Df(2L)cl-h4) (Reiff et al., 2002)
Detailed Description
	Statement Reference In homozygous GluRIIA^AD9 mutants all A-type receptors are absent, whereas B-type receptor clusters are still present in the neuromuscular junction. Latrunculin A treatment of GluRIIA^AD9 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 GluRIIA^AD9 mutants. The mean sEJC amplitude in GluRIIA^AD9 mutants is approximately one-half the amplitude of wild-type animals, consistent with complete and specific loss of A-type receptors. (Chen et al., 2005) The morphological development of neuromuscular junctions (NMJs) in GluRIIA^AD9/Df(2L)cl-h4 mutants is indistinguishable from wild type when larvae are reared at 18 or 25^oC. However, when wild-type larvae are raised at 29^oC, size-matched animals show consistently larger and more complex NMJs with more boutons. This bouton outgrowth does occur in GluRIIA^AD9/Df(2L)cl-h4 mutants reared at 29^oC, but to a much lower extent than wild type. At 29^oC, GluRIIA^AD9/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. (Sigrist et al., 2003) GluRIIA^AD9/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. (Reiff et al., 2002) 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. (Petersen et al., 1997)
External Data
Linkouts
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Statement Reference GluRIIA^AD9 has neurophysiology defective phenotype, suppressible by pAbp^k10109 (Sigrist et al., 2002)
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement Reference The elimination of one copy of GluRIIA in pAbp^k10109/+, GluRIIA^AD9/+ 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. (Sigrist et al., 2002)
Xenogenetic Interactions
Statement Reference Scer\GAL4[elav-C155]-mediated expression of Avic\GFP[Cameleon2.0.Scer\UAS] does not affect the neurological phenotype of GluRIIA[AD9] mutants. (Reiff et al., 2002)
Complementation & Rescue Data
Comments
Stocks ( 0 )

Notes on Origin
Discoverer

Comments
	Null allele. (Petersen et al., 1997)
External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 6 )
Reported As
Symbol Synonym	dglurIIA^AD9 (Sigrist et al., 2002) DGluRIIA^AD9 (Marrus et al., 2004) dglurIIA^g9 (Sigrist et al., 2003) dglur-IIA^g9 (Reiff et al., 2002) Glu-RIIA^AD9 GluRIIA^AD9 (Chen et al., 2005, Ganesan et al., 2011)
Name Synonym
Secondary FlyBase IDs

References ( 8 )
Research paper	Ganesan et al., 2011, RNA Biol. 8(5): 771--781 Drosophila glutamate receptor mRNA expression and mRNP particles. [FBrf0217952] Chen et al., 2005, J. Neurosci. 25(28): 6667--6675 The 4.1 protein coracle mediates subunit-selective anchoring of Drosophila glutamate receptors to the postsynaptic actin cytoskeleton. [FBrf0187898] Marrus et al., 2004, J. Neurosci. 24(6): 1406--1415 Differential localization of glutamate receptor subunits at the Drosophila neuromuscular junction. [FBrf0174850] Sigrist et al., 2003, J. Neurosci. 23(16): 6546--6556 Experience-dependent strengthening of Drosophila neuromuscular junctions. [FBrf0160953] Reiff et al., 2002, J. Neurosci. 22(21): 9399--9409 Differential regulation of active zone density during long-term strengthening of Drosophila neuromuscular junctions. [FBrf0152148] Sigrist et al., 2002, J. Neurosci. 22(17): 7362--7372 The postsynaptic glutamate receptor subunit DGluR-IIA mediates long-term plasticity in Drosophila. [FBrf0152143] DiAntonio et al., 1999, J. Neurosci. 19(8): 3023--3032 Glutamate receptor expression regulates quantal size and quantal content at the Drosophila neuromuscular junction. [FBrf0107675] Petersen et al., 1997, Neuron 19(6): 1237--1248 Genetic analysis of glutamate receptors in Drosophila reveals a retrograde signal regulating presynaptic transmitter release. [FBrf0100204]

Allele Dmel\GluRIIAAD9

Allele Dmel\GluRIIA^AD9