Amino acid replacement: R207K.
Nucleotide substitution: G1933A.
G12617827A
G1933A
R207K | Galphaq-PA; R207K | Galphaq-PC; R207K | Galphaq-PD; R207K | Galphaq-PE; R207K | Galphaq-PG; R250K | Galphaq-PJ; R207K | Galphaq-PK
R207K
Gαq1370/+ mutant larvae show a small decrease in quantal size. A compensatory increase in quantal content means that evoked neurotransmission is unaffected.
Homozygotes die as either first or early second instar larvae.
Animals containing large homozygous clones in the antenna have normal numbers of trichoidea, coeloconica, and basiconica sensilla. The morphology and axonal projections of olfactory sensory neurons appear normal in these animals.
The electroantennograms of animals containing large homozygous clones in the antenna have a reduced amplitude compared to controls in response to a number of odours (ethyl acetate, butanol, propionic acid, benzaldehyde and iso-amyl acetate).
The electroantennograms of Gα49B1370/+ animals show a small but significant decrease in amplitude compared to controls in response to a number of odours (ethyl acetate, butanol, propionic acid, benzaldehyde and iso-amyl acetate).
The response to ethyl acetate of ab2 large basiconic hairs that are located within homozygous clones in the antenna is significantly different from that of control cells; the firing frequency of the mutant ab2a neuron in response to ethyl acetate is strongly reduced compared to controls.
Gα49B1/Gα49B1370 flies do not show any defects in electroantennogram recordings.
Gαq1370 has abnormal neurophysiology | dominant phenotype, enhanceable by Plc21C[+]/Plc21CA
Gαq1370 has abnormal neurophysiology | dominant phenotype, enhanceable by Plc21Ck31911/Plc21C[+]
Gα49B[+]/Gαq1370 is an enhancer of abnormal neurophysiology | dominant phenotype of Plc21Ck31911
Gα49B[+]/Gαq1370 is an enhancer of abnormal neurophysiology | dominant phenotype of Plc21CA
Gα49B[+]/Gαq1370 is a suppressor of abnormal neurophysiology phenotype of rdgA1
Gα49B[+]/Gαq1370 is a suppressor of abnormal neurophysiology phenotype of rdgA3
Gαq1370/Galphaq[+], GluRIIASP16 has abnormal neurophysiology phenotype
One copy of Gαq1370 partially prevents the compensatory increase in quantal content seen in the NMJs of GluRIIASP16 mutant larvae with reduced quantal size, resulting in impaired evoked neurotransmission. These is some increase in quantal content compared with Gαq1370/+ controls, but not enough to compensate for the reduced quantal size.
The electroantennograms of Gα49B1370/Plc21CA and Gα49B1370/Plc21Ck31911 double heterozygous animals show a significant decrease in amplitude compared to controls in response to a number of odours (ethyl acetate, butanol, propionic acid, benzaldehyde and iso-amyl acetate) and the reduction in the double heterozygotes is significantly greater than that expected to arise from a mere additive effect of the single heterozygous phenotypes.
Introduction of a single copy of Gα49B1370 to rdgA1 or rdgA3 homozygotes significantly rescues the electroantennogram responses of the homozygotes.
Gαq1370 is rescued by Scer\GAL4Orco.2.642.Hsim\VP22/GαqUAS.cRa
Expression of Gα49BScer\UAS.cRa under the control of Scer\GAL4Or83b.2.642.T:Hsim\VP22 rescues the reduced electroantennogram amplitude in response to odours of animals containing large Gα49B1370 homozygous clones in the antenna.
Expression of Gα49BScer\UAS.cRa under the control of Scer\GAL4Or83b.2.642.T:Hsim\VP22 only during adulthood (expression is inhibited before this stage by expression of Scer\GAL80ts.αTub84B at 18[o]C, and the animals are shifted to 29[o]C to inactivate Scer\GAL80ts.αTub84B a few hours before eclosion) also rescues the reduced electroantennogram amplitude in response to odours of animals containing large Gα49B1370 homozygous clones in the antenna.