One copy of Gαq221c prevents the compensatory increase in quantal content seen in the NMJs of GluRIIASP16 mutant larvae with reduced quantal size, resulting in impaired evoked neurotransmission. There is no increase in quantal content compared with Gαq221c/+ controls.
The electroantennograms of Gα49B221c/Plc21CA and Gα49B221c/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.
The viability of Itp-r83Awc703/Itp-r83Awc361 animals is unaffected by Gα49B221c/+, but the resulting adults have abnormal wing posture, an enhanced incidence of flight defects and mild endogenous hyperactivity of spontaneous firing recorded from the dorsal longitudinal muscles. Wing posture and flight defect phenotypes are enhanced and viability is reduced if Plc21Ck31911/+ is also present but partially suppressed by Gα49BScer\UAS.cRa; Scer\GAL4Ddc.PL and completely or largely suppressed by Ca-P60AKum170/+, even when Plc21Ck31911/+ is also present.
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 Gα49B221c 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 Gα49B221c homozygous clones in the antenna.