|Feature type||allele||Associated gene||Dmel\Gαs|
|Also Known As||dgsR60, dgsR60c|
|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|
Nucleotide substitution: T723A. Amino acid replacement: Y241@.
|Phenotype Manifest In|
Homozygous ab1C olfactory receptor neurons (ORNs) generated using MARCM show normal responses to CO[] in 6 day old flies. A decrease in CO[] response is observed in these neurons in 20 day old flies, at all concentrations of CO[] 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-sα60A[R60]/+ flies than in wild-type controls. This effect is not seen with lower concentrations of trehalose.
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.
|Phenotype Manifest In|
|Complementation & Rescue Data|
|Partially rescued by|
|Not rescued by|
Expression of G-sα60A[Scer\UAS.cCa] under the control of Scer\GAL4[Orco.T:Hsim\VP16] in homozygous G-sα60A[R60] 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.
|Stocks ( 1 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 9 )|
|Secondary FlyBase IDs|
|References ( 8 )|
|Personal communication to FlyBase|