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General Information
Symbol
Dmel\mGluR112b
Species
D. melanogaster
Name
FlyBase ID
FBal0213218
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
dmGluRA112b, DmGluRA112, mGluRA112b, Glu-RA112b
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Cytology
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.

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 ( 1 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

mGluR112b mutants have an altered daily sleep profile, with: increased sleep during daytime and reduced sleep during nighttime; increased sleep bout number, but not duration, during daytime and decreased number of longer (>15min) sleep bouts during nighttime; increased number and decreased duration of wake bouts only during daytime, and decreased duration of wake bouts during nighttime. However, there are no significant changes in: total daily sleep amounts, waking activity or climbing ability (negative geotaxis) when compared to wild-type controls.

In mGluR112b mutants, after multiple days under constant darkness, the sleep and wake rhythms, the sleep amount during the subjective day and night, as well as sleep and wake bouts become similar to those in controls. Some of these changes are already observed after 2 days in constant dark.

At one month of age, mGluR112b mutants exhibit increased sleep, higher sleep bouts with no change in average length of sleep bouts, and more wake bouts with decreased wake bout length during day time while at night, they exhibit decreased sleep, reduced sleep bout length with a reduction in number of sleep bouts and fewer wake bouts with increased bout length when compared to aged controls. Also they show reduced total daily sleep amount when compared to aged controls.

mGluR112b mutant flies are deficient in olfactory short term memory compare to controls.

mGluR112b/mGluR112b mutant males between 6-10 days post-eclosion have significantly impaired courtship behavior, exhibiting almost no courtship activity, as compared with mGluR2b/mGluR2b controls, and are defective in progressing through the phases of courtship, but do not display any gross defects in locomotor behavior, olfaction or vision, as compared to wild type.

mGluR112b/+ mutant males exhibit significantly impaired courtship behavior; and impaired learning-during-training, immediate-recall memory, short-term memory or long-term memory in conditioned courtship assays, but no significant defects in progressing through the phases of courtship, and do not display any gross defects in locomotor behavior, olfaction or vision, as compared to wild type.

Boutons in mGluRA112b mutants often appear to be larger in size than wild-type.

mGluRA112b mutants exhibit neuronal hyper-excitability and demonstrate an increase rate of onset of long term facilitation.

mGluR112b/+ 30-day-old adult males display learning defects (fail to demonstrate the typical decrease in courtship activity when paired with an mated unreceptive female) as well as the loss of short-term (60 min) memory.

mGluRA112b mutants show a tendency towards elevated response amplification compared to controls. However, there are no statistically significant differences in EJC amplitude between mGluRA112b and controls.

mGluRA112b mutants show comparable levels of short-term facilitation as wild-type controls.

During prolonged 10-Hz stimulation, mGluRA112b mutants exhibit a large increase in mean normalised response amplitude during the entire period of prolonged high-frequency stimulation (HFS). During early HFS (<10s), mGluRA112b mutants quickly reach their augmentation peak amplitude.

mGluRA112b mutants exhibit a striking hyperpotentiation response amplitude. This is transient, persisting on average for 30 seconds following HFS.

mGluRA112b 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.

Loss of mGluR through a mGluR112b null mutant background strongly impairs coordinated movement behavior, with the average response time in a roll-over assay lengthened by 48%. In individual animals, the behavioral defect is clearly evident as a combination of inappropriate movement responses and defects in cooperative motor control. These mutants appear to 'struggle' during a period of continuous spastic muscle contraction. mGluR112b mutant larvae display a very significantly slowed performance compared to wild-type.

mGluR112b mutants display no defects in neuromuscular junction synaptic branching, compared to wild-type.

mGluR112b mutants display a slight, but not quite significant decrease in synaptic area compared to controls.

mGluR112b mutants display a small decrease in the number of synaptic boutons in the neuromuscular junction.

At the ultrastructural level, the overall appearance of a bouton and the postsynaptic subsynaptic reticulum in mGluR112b mutants appears normal. Quantitatively, there is no significant difference in bouton size, mitochondria size, active zone size/number or the postsynaptic subsynaptic reticulum between mGluR112b mutants and control larvae.

The functional properties of glutamergic neuromuscular junctions from mGluRA112b 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 mGluRA112b larvae.

Using a stimulation frequency of 10 Hz, the level of facilitation during short stimulus trains is increased approximately threefold on average in mGluRA112b larval neuromuscular junctions compared with controls. During prolonged stimulation at 5 Hz, the response pattern dramatically changes in mGluRA112b 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. mGluRA112b/Df(4)O2 larvae also show this phenotype.

Third star mutant mGluRA112b/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. mGluRA112b/+ larvae do not show defects in bouton number or size.

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

mGluR112b is an enhancer of terminal bouton phenotype of Fmr1Δ50M

Suppressor of
Statement
Reference

mGluR112b is a suppressor of synaptic vesicle phenotype of Fmr1Δ50M

NOT Suppressor of
Statement
Reference

mGluR112b is a non-suppressor of synapse phenotype of Fmr1Δ50M

mGluR112b is a non-suppressor of presynaptic active zone phenotype of Fmr1Δ50M

Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

Drep2ex13 mGluR112b double mutants exhibit olfactory short term memory defects similar to those seen in either mutant alone.

CaMKIIT287D.Scer\UAS expression completely suppresses the hyper-excitability found in mGluRA112b mutants to the level found upon expression of CaMKIIT287D.Scer\UAS in a wild-type background.

The age-onset learning and memory defects (measured in a courtship behavior assay) characteristic for both PsnI2 and PsnB3 heterozygote males are suppressed by combination with a single copy of the mGluR112b allele.

Fmr13;mGluRA112b double mutants do not exhibit any difference in EJC response amplitude compared to Fmr13 or mGluRA112b single mutants and wild-type controls.

Fmr13;mGluRA112b double mutants manifest greatly elevated faciliataion during 20Hz high-frequency stimulation, indicating a synergistic interaction leading to enhanced short-term facilitation in Fmr13;mGluRA112b double mutants.

During prolonged 10-Hz stimulation, Fmr13;mGluRA112b 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 mGluRA112b single mutants. During early HFS (<10s), Fmr13;mGluRA112b 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 mGluRA112b hyperpotentiation response is strongly reduced in Fmr13; mGluRA112b 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 mGluRA112b single mutant.

Fmr13; mGluRA112b double mutants, as with mGluRA112b 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. Fmr13; mGluRA112b double mutants oscillate between the augmented and LTF states.

The high level of homosexual courtship behaviour that is seen in gbKG07905 males is partially suppressed if they are also mutant for mGluRA112b.

A Fmr1Δ50M mutant background suppresses the behavioral/movement impairment seen in mGluR112b mutant larva. In these double mutants the roll-over behavioral response is smooth and efficient, with a significantly shorter 'struggle' time compared to mGluR112b single mutants. Quantitatively, the double mutant shows comparable behavior to the wild-type control.

Fmr1Δ50M;mGluR112b double mutants display some suppression of the Fmr1Δ50M single mutant synaptic overbranching phenotype but the level of overbranching is still significant compared to wild-type controls.

Fmr1Δ50M;mGluR112b double mutants do not show any suppression of the increased neuromuscular junction synaptic area characteristic of Fmr1Δ50M single mutants.

Fmr1Δ50M;mGluR112b double mutants display a synergistic increase in synaptic bouton number compared to Fmr1Δ50M single mutants.

Fmr1Δ50M;mGluR112b double mutants show a significant rescue of the elevated vesicle density phenotype seen in Fmr1Δ50M single mutants. This includes the clustered vesicles around the active zone.

A Fmr13 mutant background suppresses the behavioral/movement impairment seen in mGluR112b mutant larva. In these double mutants the roll-over behavioral response is smooth and efficient, with a significantly shorter 'struggle' time compared to mGluR112b single mutants. Quantitatively, the double mutant shows comparable behavior to the wild-type control.

eag1, Sh120; mGluRA112b show the neuromuscular junction overgrowth phenotype of eag1, Sh120 double mutants.

mGluRA112b/+; Gβ13FΔ1-96A/+ 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.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
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Mutant
Wild-type
Stocks (0)
Notes on Origin
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External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (7)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (11)