|Feature type||allele||Associated gene||Dmel\mGluRA|
|Also Known As||DmGluRA112b|
|Allele class||loss of function allele|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
|Phenotype Manifest In|
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.
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.
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.
|NOT Enhanced by|
mGluRA112b is a suppressor | partially of courtship behavior defective | male phenotype of gbKG07905
|Phenotype Manifest In|
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.
Fmr1;mGluRA[112b] double mutants do not exhibit any difference in EJC response amplitude compared to Fmr1 or mGluRA[112b] single mutants and wild-type controls. Fmr1;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;mGluRA[112b] double mutants. During prolonged 10-Hz stimulation, Fmr1;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;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; 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; 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; mGluRA[112b] 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.
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.
|Complementation & Rescue Data|
|Not rescued by|
|Stocks ( 0 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 3 )|
|Secondary FlyBase IDs|
|References ( 4 )|