Amino acid replacement: Y241term.
Nucleotide substitution: T723A.
T23945997A
T723A
Y241term | Galphas-PA; Y241term | Galphas-PB; Y241term | Galphas-PC; Y241term | Galphas-PD; Y241term | Galphas-PE
Y241term
Homozygous ab1C olfactory receptor neurons (ORNs) generated using MARCM show normal responses to CO[[2]] in 6 day old flies. A decrease in CO[[2]] response is observed in these neurons in 20 day old flies, at all concentrations of CO[[2]] tested.
Homozygous ab3A ORNs generated using MARCM show a normal odour response to low concentrations of either methyl butyrate (0.05% and lower) or butyric acid (1% and lower). However, at near saturating concentrations, there is a small decrease in the odour response for both these odorants.
Uptake of 40-80mM trehalose solution is significantly lower in G-sα60AR60/+ flies than in wild-type controls. This effect is not seen with lower concentrations of trehalose.
GαsR60 mutant flies show resistance to V. cholerae infection compared to controls.
Somatic clones of G-sα60AR60 homozygous cells persist in the adult wing blade after surrounding heterozygous or wild-type cells have died.
Low-frequency nerve stimulation at 0.5 mM Ca2+ evokes robust synaptic currents in G-sα60AR60 embryos. However, at 0.2 mM Ca2+ nerve stimulation often fails to evoke synaptic currents in homozygous G-sα60AR60 embryos while currents are evoked in G-sα60AR60/+ embryos. G-sα60AR60 mutants show minimal synaptic facilitation during tetanic stimulation and lack of post-tetanic potentiation, compared to G-sα60AR60/+ embryos. Additionally, during and after tetanus, asynchronous transmitter release is not enhanced to the same levels in G-sα60AR60 homozygotes as in G-sα60AR60/+ heterozygotes. Miniature synaptic currents (mSCs) are smaller in amplitude and less frequent in G-sα60AR60 embryos when tested in saline with normal concentrations of K+ than in heterozygotes. In high concentrations of K+ saline, G-sα60AR60 embryos produce less frequent mSCs with smaller average amplitudes and the amplitude distribution is skewed toward larger amplitudes compared to G-sα60AR60/+ embryos. The mean amplitude of glutamate-induced inward currents is not different in G-sα60AR60 homozygotes and heterozygotes, showing that the total number of postsynaptic receptors is not different. Additionally, the unitary glutamate receptor channel current is not different and the pre-synaptic receptors for metabotropic glutamate and octopamine do not have an altered response in G-sα60AR60 embryos.
38% of homozygous embryos die (the percentage of embryos dying is not increased if they are derived from females carrying homozygous germ-line clones), the remaining homozygous larvae die either as they hatch or shortly after hatching. Larvae that hatch show little or no movement and do not grow. Ovaries of females carrying homozygous germ-line clones appear normal. 11% of G-sα60AR60/G-sα60AR19 embryos die. 44% of G-sα60AR60/G-sα60AR19 embryos derived from females carrying G-sα60AR60 homozygous germ-line clones die. 27% of G-sα60AR60/Df(2R)or-BR11 embryos die. 48% of G-sα60AR60/Df(2R)or-BR11 embryos derived from females carrying G-sα60AR60 homozygous germ-line clones die. G-sα60AR60/G-sα60AR19 embryos derived from females carrying G-sα60AR60 or G-sα60AR19 homozygous germ-line clones do not have cuticle defects.
GαsR60/G-salpha60A[+] is an enhancer of wing margin phenotype of Bx2
GαsR60/G-salpha60A[+] is a suppressor of scutellar bristle | increased number phenotype of Chie5.5
GαsR60/G-salpha60A[+] is a suppressor of scutellar bristle | increased number phenotype of SsdpL7
GαsR60 is rescued by GαsUAS.cCa/Scer\GAL4VP16.Orco
GαsR60 is partially rescued by GαsW24.UAS/Scer\GAL4elav.PLu
GαsR60 is not rescued by Scer\GAL4Mhc.PW/GαsW24.UAS
Expression of G-sα60AScer\UAS.cCa under the control of Scer\GAL4Orco.T:Hsim\VP16 in homozygous G-sα60AR60 ab3A olfactory receptor neurons rescues the reduced odour response seen in these neurons at near saturating concentrations of either methyl butyrate or butyric acid.
Expression of one copy of G-sα60A+t10 is able to rescue some aspects of the synaptic impairment in G-sα60AR60 homozygote mutant embryos, while it fails to rescue other aspects. For example, G-sα60A+t10 partially rescues the synaptic facilitation during tetanic stimulation defect, it enhances the asynchronous transmitter release during and after tetanus and it increases the frequency and amplitude of mSCs. However, embryos expressing G-sα60A+t10 still show a failure to evoke synaptic currents in response to nerve stimulation, they still lack post-tetanic potentiation and still exhibit a skewed amplitude distribution. Expression of G-sα60AW24.Scer\UAS in neurons, driven by Scer\GAL4elav.PLu, restores many synaptic defects in G-sα60AR60 embryos. One notable exception is that post-tetanic potentiation is not as strong as that observed in heterozygous G-sα60AR60 embryos. In contrast, when G-sα60AW24.Scer\UAS is expressed in muscle, driven by Scer\GAL4Mhc.PW, it completely fails to rescue the synaptic impairment seen in G-sα60AR60 embryos.
Null allele.