Imprecise excision of P{SUPor-P}Gα49BKG07290 has produced a 359bp deletion in the region of the Gα49B translation start site.
Gαq221c/+ mutant larvae show a small decrease in spontaneous miniature neurotransmission. A compensatory increase in quantal content means that evoked neurotransmission is unaffected.
1 day old flies in which the whole eye is mutant for Gα49B221c do not show any detectable rhabdomere defects.
Homozygous ab3A ORNs generated using MARCM show a normal odour response to methyl butyrate and to butyric acid.
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 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 Gα49B221c/+ 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).
Gα49B1/Gα49B221c flies do not show any defects in electroantennogram recordings.
Gα49Bf04219 homozygotes die at around 10-12 hours post-hatching.
Gαq221c has abnormal neurophysiology | dominant phenotype, enhanceable by Plc21C[+]/Plc21CA
Gαq221c has abnormal neurophysiology | dominant phenotype, enhanceable by Plc21Ck31911/Plc21C[+]
Gα49B[+]/Gαq221c, Itprwc703/Itprwc361 has flightless | partially phenotype, enhanceable by Plc21Ck31911/Plc21C[+]
Gα49B[+]/Gαq221c, Itprwc703/Itprwc361 has flightless | partially phenotype, suppressible by Ca-P60A[+]/SERCAKum170
Gα49B[+]/Gαq221c, Itprwc703/Itprwc361, Plc21Ck31911/Plc21C[+] has flightless | partially phenotype, suppressible by Ca-P60A[+]/SERCAKum170
Gα49B[+]/Gαq221c, Itprwc703/Itprwc361 has abnormal neurophysiology phenotype, suppressible by Ca-P60A[+]/SERCAKum170
Gα49B[+]/Gαq221c, Itprwc703/Itprwc361, Plc21Ck31911/Plc21C[+] has abnormal neurophysiology phenotype, suppressible by Ca-P60A[+]/SERCAKum170
Gα49B[+]/Gαq221c, Itprwc703/Itprwc361 has flightless | partially phenotype, suppressible | partially by GαqUAS.cRa/Scer\GAL4Ddc.PL
Gα49B[+]/Gαq221c, Itprwc703/Itprwc361 has abnormal neurophysiology phenotype, suppressible | partially by GαqUAS.cRa/Scer\GAL4Ddc.PL
Gαq221c/Galphaq[+] is an enhancer | female limited of partially lethal - majority die phenotype of Scer\GAL4elav-C155, cacRQ,SL.UAS.EGFP
Galpha49B[+]/Gαq221c is an enhancer of abnormal neurophysiology | dominant phenotype of Plc21Ck31911
Galpha49B[+]/Gαq221c is an enhancer of abnormal neurophysiology | dominant phenotype of Plc21CA
Gα49B[+]/Gαq221c is an enhancer of flightless | partially phenotype of Itprwc703/Itprwc361
Galpha49B[+]/Gαq221c is a suppressor of abnormal neurophysiology phenotype of rdgA3
Galpha49B[+]/Gαq221c is a suppressor of abnormal neurophysiology phenotype of rdgA1
Gαq221c/Galphaq[+], GluRIIASP16 has abnormal neurophysiology phenotype
Gα49B[+]/Gαq221c, Itprwc703/Itprwc361, Plc21Ck31911/Plc21C[+] has partially lethal - majority die phenotype
Gα49B[+]/Gαq221c, Itprwc703/Itprwc361 has abnormal neurophysiology phenotype
Gα49B[+]/Gαq221c, Itprwc703/Itprwc361 has wing phenotype, enhanceable by Plc21Ck31911/Plc21C[+]
Gα49B[+]/Gαq221c, Itprwc703/Itprwc361 has wing phenotype, suppressible by Ca-P60A[+]/SERCAKum170
Gα49B[+]/Gαq221c, Itprwc703/Itprwc361 has wing phenotype, suppressible | partially by GαqUAS.cRa/Scer\GAL4Ddc.PL
Gα49B[+]/Gαq221c, Itprwc703/Itprwc361, Plc21Ck31911/Plc21C[+] has wing phenotype, suppressible by Ca-P60A[+]/SERCAKum170
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.
Introduction of a single copy of Gα49B221c to rdgA1 or rdgA3 homozygotes significantly rescues the electroantennogram responses of the homozygotes.
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.
Gαq221c 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 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.