Allele Dmel\mGluRA^112b

General Information
Symbol	Dmel\mGluRA^112b	Species	D. melanogaster
Name		FlyBase ID	FBal0213218
Feature type	allele	Associated gene	Dmel\mGluRA
Also Known As	DmGluRA^112b

Allele class	loss of function allele
Mutagen	Delta2-3
Recent Updates
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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 (Bogdanik et al., 2004)
Mutagen	Delta2-3 (Bogdanik et al., 2004)
Mutations Mapped to the Genome

Type Location Additional Notes References
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype	P{hsp26-pt-T}39C-42 (Bogdanik et al., 2004)
Nature of the lesion	Statement Reference Imprecise excision of the P{hsp26-pt-T} element, resulting in deletion of the putative transcription start, the start codon, plus part of the coding sequence of the mGluRA gene. (Bogdanik et al., 2004)
Cytology
Phenotypic Data
Phenotypic Class
	neuroanatomy defective (Chun-Jen Lin et al., 2011) neuroanatomy defective \| recessive (Bogdanik et al., 2004) neurophysiology defective (Bogdanik et al., 2004, Repicky and Broadie, 2009, Chun-Jen Lin et al., 2011) neurophysiology defective (with Df(4)O2) (Bogdanik et al., 2004) viable (Bogdanik et al., 2004)
Phenotype Manifest In
	bouton (Chun-Jen Lin et al., 2011) type I bouton (Bogdanik et al., 2004) type I bouton (with Df(4)O2) (Bogdanik et al., 2004)
Detailed Description
	Statement Reference Boutons in mGluRA[112b] mutants often appear to be larger in size than wild-type. mGluRA[112b] mutants exhibit neuronal hyper-excitability and demonstrate an increase rate of onset of long term facilitation. (Chun-Jen Lin et al., 2011) mGluRA[112b] mutants show a tendency towards elevated response amplification compared to controls. However, there are no statistically significant differences in EJC amplitude between mGluRA[112b] and controls. mGluRA[112b] mutants show comparable levels of short-term facilitation as wild-type controls. During prolonged 10-Hz stimulation, mGluRA[112b] mutants exhibit a large increase in mean normalised response amplitude during the entire period of prolonged high-frequency stimulation (HFS). During early HFS (<10s), mGluRA[112b] mutants quickly reach their augmentation peak amplitude. mGluRA[112b] mutants exhibit a striking hyperpotentiation response amplitude. This is transient, persisting on average for 30 seconds following HFS. mGluRA[112b] mutants show premature LTF, manifested as a sudden increase in EJC response amplitude during HFS.The transition between the modestly elevated augmentation level and the dramatically elevated LTF level is very sharp, usually occurring in a single jump between two adjacent stimiuli. This change is always unidirectional to the hyper-facilitated level, which persists for the length of the HFS and beyond. (Repicky and Broadie, 2009) The functional properties of glutamergic neuromuscular junctions from mGluRA^112b wandering third instar larvae show no changes in basal synaptic transmission compared to controls. Also, the response patterns of synapses in the presence of 1.8mM Ca²⁺ is undistinguishable between mutants and controls. Action potential propagation in motor nerves appears unaffected in mGluRA^112b larvae. Using a stimulation frequency of 10 Hz, the level of facilitation during short stimulus trains is increased approximately threefold on average in mGluRA^112b larval neuromuscular junctions compared with controls. During prolonged stimulation at 5 Hz, the response pattern dramatically changes in mGluRA^112b mutants showing a step-like, 10-fold increase in EJC amplitude that is accompanied by pronounced asynchrony of the response. After stimulation, synaptic responses remain strongly potentiated in mutants before they suddenly revert to a normal level of sustained posttetanic potentiation. mGluRA^112b/Df(4)O2 larvae also show this phenotype. Third star mutant mGluRA^112b/Df(4)O2 and neuromuscular junctions show a significant reduction in the number of type I synaptic boutons compared to controls. The mutant Ib boutons are larger in size than in controls, although the total area covered by the boutons is the same as in controls, indicating a compensation of the defect in bouton number by an increase in size. mGluRA^112b/+ larvae do not show defects in bouton number or size. (Bogdanik et al., 2004)
External Data
Linkouts
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement Reference mGluRA^112b has neurophysiology defective phenotype, enhanceable by Fmr1³ (Repicky and Broadie, 2009)
NOT Enhanced by
Statement Reference mGluRA^112b has neurophysiology defective phenotype, non-enhanceable by Fmr1³ (Repicky and Broadie, 2009)
Suppressed by
Statement Reference mGluRA^112b has neurophysiology defective phenotype, suppressible by CaMKII^{T287D.Scer\UAS}/Scer\GAL4^D42 (Chun-Jen Lin et al., 2011)
Suppressor of
Statement Reference mGluRA^112b is a suppressor \| partially of courtship behavior defective \| male phenotype of gb^KG07905 (Grosjean et al., 2008) mGluRA^112b is a suppressor of neurophysiology defective phenotype of Fmr1³ (Repicky and Broadie, 2009)
Phenotype Manifest In
Other
Statement Reference Gbeta13F[+]/Gβ13F^Δ1-96A, mGluRA^112b has bouton phenotype (Bogdanik et al., 2004)
Additional Comments
Genetic Interactions
Statement Reference CaMKII[T287D.Scer\UAS] expression completely suppresses the hyper-excitability found in mGluRA[112b] mutants to the level found upon expression of CaMKII[T287D.Scer\UAS] in a wild-type background. (Chun-Jen Lin et al., 2011) Fmr1[3];mGluRA[112b] double mutants do not exhibit any difference in EJC response amplitude compared to Fmr1[3] or mGluRA[112b] single mutants and wild-type controls. Fmr1[3];mGluRA[112b] double mutants manifest greatly elevated faciliataion during 20Hz high-frequency stimulation, indicating a synergistic interaction leading to enhanced short-term facilitation in Fmr1[3];mGluRA[112b] double mutants. During prolonged 10-Hz stimulation, Fmr1[3];mGluRA[112b] double mutants exhibit a large increase in mean normalised response amplitude during the entire period of prolonged high-frequency stimulation (HFS). However, this is no greater than in mGluRA[112b] single mutants. During early HFS (<10s), Fmr1[3];mGluRA[112b] double mutants exhibit a drastically slower increase in response amplitude than single mutants, although the elevated augmentation is similar during later periods as HFS continues. The mGluRA[112b] hyperpotentiation response is strongly reduced in Fmr1[3]; mGluRA[112b] double mutants, with response amplitudes comparable to controls. There is a four-fold decrease in the duration of the hyperpotentiated responses in the double mutant compared with the mGluRA[112b] single mutant. Fmr1[3]; mGluRA[112b] double mutants, as with mGluRA[112b] mutants, show premature LTF, manifested as a sudden increase in EJC response amplitude during HFS. These double mutants manifest a clear difficulty in surpassing the LTF threshold. Fmr1[3]; mGluRA[112b] double mutants oscillate between the augmented and LTF states. (Repicky and Broadie, 2009) The high level of homosexual courtship behaviour that is seen in gb^KG07905 males is partially suppressed if they are also mutant for mGluRA^112b. (Grosjean et al., 2008) eag¹, Sh¹²⁰; mGluRA^112b show the neuromuscular junction overgrowth phenotype of eag¹, Sh¹²⁰ double mutants. mGluRA^112b/+; Gβ13F^Δ1-96A/+ double mutant larvae show an increase in synaptic bouton size that is not seen in either single mutant heterozygote. The bouton number is not changed in the double mutants. (Bogdanik et al., 2004)
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Rescued by	mGluRA^112b is rescued by mGluRA^Scer\UAS.cRa/Scer\GAL4^BG380 (Bogdanik et al., 2004)
Not rescued by	mGluRA^112b is not rescued by mGluRA^Scer\UAS.cRa/Scer\GAL4^Mhc.PW (Bogdanik et al., 2004)
Comments
Stocks ( 0 )

Notes on Origin
Discoverer

External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 3 )
Reported As
Symbol Synonym	DmGluRA^112b (Bogdanik et al., 2004) dmGluRA^112b (Repicky and Broadie, 2009) mGluRA^112b (Grosjean et al., 2008, Chun-Jen Lin et al., 2011)
Name Synonym
Secondary FlyBase IDs

References ( 4 )
Research paper	Chun-Jen Lin et al., 2011, Genetics 188(3): 601--613 The Metabotropic Glutamate Receptor Activates the Lipid Kinase PI3K in Drosophila Motor Neurons Through the Calcium/Calmodulin-Dependent Protein Kinase II and the Nonreceptor Tyrosine Protein Kinase DFak. [FBrf0214227] Repicky and Broadie, 2009, J. Neurophysiol. 101(2): 672--687 Metabotropic glutamate receptor-mediated use-dependent down-regulation of synaptic excitability involves the fragile x mental retardation protein. [FBrf0206949] Grosjean et al., 2008, Nat. Neurosci. 11(1): 54--61 A glial amino-acid transporter controls synapse strength and courtship in Drosophila. [FBrf0201004] Bogdanik et al., 2004, J. Neurosci. 24(41): 9105--9116 The Drosophila metabotropic glutamate receptor DmGluRA regulates activity-dependent synaptic facilitation and fine synaptic morphology. [FBrf0180430]

Allele Dmel\mGluRA112b

Allele Dmel\mGluRA^112b