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General Information
Symbol
Dmel\Gαq1
Species
D. melanogaster
Name
FlyBase ID
FBal0052412
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
dgq1, Gαq1, Gαq1, Gα49B1, Gaq1, Gαq1
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:

G12617071A

Comment:

G to A nucleotide change maps to a splice acceptor site. Results in the use of a cryptic splice site 9 nucleotides downstream, causing an in-frame deletion of 3 codons encompassing amino acid residues 154-156.

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Nucleotide substitution: G1910A. Alteration maps to the splice acceptor site at the intron 3-exon 4 boundary. Causes use of a cryptic splice site 9 nucleotides downstream, causing an in-frame deletion of 3 codons encompassing amino acid residues 154-156.

Expression Data
Reporter Expression
Additional Information
Statement
Reference
 
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

At six days in light/dark cycles, Gαq1 mutants do not yet display appreciable signs of retinal degeneration. Gαq1 flies show substantial but much weaker electroretinogram response to light stimulation (even a very bright illumination) as compared to wild-type controls.

Gαq1 homozygous (and with a lower penetrance also heterozygous) third instar larvae display high frequency of ectopic targetting of type III axons to the abdominal body-wall muscle 13.

Gαq1 homozygous mutant late third instar larvae show impaired temperature selection and unlike controls display no strong preference for cooler temperatures (18[o]C) in a temperature gradient.

The gustatory aversion of mutant flies to 6mM camphor in a two way-choice test is not significantly different from that seen in wild-type flies.

Gα49B1/Gα49B961 adults show a defective electroretinogram response.

The minimum light intensity needed to induce a prolonged depolarization afterpotential is much lower than normal in mutant flies.

Mutants undergo slow light-dependent retinal degeneration.

The citronellal-evoked action potential frequency in ab12 basiconic sensilla in the antenna of mutant flies is not significantly different from wild type.

Mutant flies show significantly reduced avoidance of citronellal in a direct airborne repellent test (DART) assay.

ab11a olfactory receptor neurons (ORNs) in the antenna show a higher citronellal-evoked action potential frequency in mutant flies compared to in wild type.

Gα49B1 flies show a normal lifespan on dead yeast medium, but show reduced survival compared to controls on live yeast medium. The gut cells of the mutant flies fed on live yeast medium show severe apoptosis (the gut cells of mutant flies fed on dead yeast medium do not show severe apoptosis).

Gα49B1 flies show a 100-fold increase in the number of yeast colony-forming units (CFUs) in the gut compared to control flies when fed on live yeast medium.

Gα49B1/Gα49B221c and Gα49B1/Gα49B1370 flies do not show any defects in electroantennogram recordings.

The preference to choose 18[o]C over 24[o]C is greatly reduced in Gα49B1 mutants. Gα49B1 larvae are able to select 18[o]C over uncomfortably cool (14-16[o]C) and uncomfortably warm temperatures (26-32[o]C).

The rhabdomeres of 7 day old mutant flies have no obvious morphological changes relative to wild type.

In Gα49B1/Df(2R)vg135 mutants, internalisation of trplninaE.T:Avic\GFP-EGFP into photoreceptor cells is strongly inhibited. On average, in 3.65 photoreceptor cells per ommatidium trplninaE.T:Avic\GFP-EGFP remains in the rhabdomeres.

Endocytosis of ninaE is normal in Gα49B1 photoreceptors.

At 10 days post eclosion, Gα49B1 retina exhibit smaller, disorganized and occasionally missing rhabdomeres relative to wild type. Gα49B1 flies raised in the light show significant retinal degeneration over 14 days, while Gα49B1 flies raised in the dark show little degeneration.

Gα49B1 has no significant effect on the visual impairment caused by exposure to constant light.

Mutant flies show no response to light (measured using an electroretinogram (ERG) recording).

Gα49B1 mutants do not exhibit the light dependent architectural changes seen in wild-type rhabdomeres.

Spontaneous quantum bumps of about 2pA in amplitude, which are detected in wild-type photoreceptors in complete darkness, are absent or greatly reduced in frequency in Gα49B1 photoreceptors. Gα49B1 photoreceptors show about a 1000-fold reduction in sensitivity to light compared to wild-type photoreceptors and mutant responses to brief light flashes decay abnormally slowly, returning to baseline with a time constant of about 100ms. The amplitude of light induced quantum bumps in the photoreceptors of Gα49B1 mutants are on average 3- to 4-fold smaller than wild-type, bump duration is reduced and the integral current is reduced about 5- to 6-fold compared to wild type (when ATP is present in the intracellular solution during recordings). When ATP is absent from the intracellular solution during recordings, the amplitude of quantum bumps from mutant photoreceptors increases to values approaching wild type.

The effect of anoxia as measured in the eye by extracellular voltage change recordings is similar to that of wild type except that the latency of onset of the larger phase of the response is twice as long as wild type.

Mutants raised in normal light show normal ommatidial structure and exhibit no loss of Deep pseudopupil.

Linolenic acid can activate light sensitive channels in mutant photoreceptors.

The size and shape of the quantum bumps are unaffected, although the frequency is significantly different from wild type.

Retina does not exhibit light-dependent degeneration. When present Gα49B1 is unable to suppress the retinal light-dependent degeneration of rdgC306 mutants.

Mutant photoreceptors show a dramatic loss of light responsiveness, displaying more than a 1000-fold loss in light sensitivity. Deactivation kinetics of the residual light response is very different from wild-type. Wild type has deactivation time constant of 19.0 +/- 5ms, compared to 127 +/- 24ms for mutant. Mutant photoreceptors display a dramatic decrease in the probability of quantum bump formation.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Statement
Reference
NOT suppressed by
Statement
Reference

Gαq1 has thermotaxis defective phenotype, non-suppressible by TrpA11

Gαq1 has neurophysiology defective phenotype, non-suppressible by Cds1

NOT Enhancer of
Statement
Reference

Galphaq[+]/Gαq1 is a non-enhancer of neuroanatomy defective | third instar larval stage phenotype of rl1

Suppressor of
Statement
Reference
Phenotype Manifest In
Enhanced by
Statement
Reference

Gαq1, rdgC306 has ommatidium phenotype, enhanceable by Arr21

Suppressed by
Statement
Reference

Gαq1 has photoreceptor cell phenotype, suppressible by rdgA3

Gαq1, rdgC306 has ommatidium phenotype, suppressible by Arr23

NOT suppressed by
Statement
Reference

Gαq1 has photoreceptor cell phenotype, non-suppressible by Cds1

NOT Enhancer of
Statement
Reference

Galphaq[+]/Gαq1 is a non-enhancer of axon | third instar larval stage phenotype of rl1

Suppressor of
Statement
Reference

Gαq1 is a suppressor of rhabdomere phenotype of tadr1

Gαq1 is a suppressor of eye photoreceptor cell phenotype of Camtates-2

Gαq1 is a suppressor | partially of rhabdomere phenotype of rdgA3

Gαq1 is a suppressor | partially of retina phenotype of ninaEpp100

Arr25/Gαq1 is a suppressor of retina phenotype of ninaEpp100

Gαq1 is a suppressor of ommatidium phenotype of Arr23

Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

Introduction of TrpA11 into a Gα49B1 background results in loss of temperature selection identical to that resulting from the Gα49B1 alone.

The reduced size of the peripheral rhabdomeres in 7 day old tadr1 flies is suppressed if they are also mutant for Gα49B1.

The Gα49B1 mutation suppresses the multiple bump phenotype seen in Camtates-2 mutant photoreceptors following stimulation with a flash of dim light.

Gβ76C1/+ ; Gα49B1/+ double mutants exhibit almost normal sensitivity to light and no spontaneous activity in the dark.

The rate of retinal degeneration in rdgA3 ; Gα49B1 double mutants is slower than that of rdgA3 single mutants.

Gα49B1; ninaEpp100 double mutant flies show a significant rescue of the ninaEpp100 retinal degeneration phenotype to the levels of Gα49B1 single mutants.

Gα49B1; Arr25, ninaEpp100 triple mutants show a suppression of the retinal degeneration phenotypes seen in ninaEpp100 single mutants. The triple mutants exhibit only very minor rhabdomeric abnormalities after 40 days.

Spontaneous currents are abolished in norpA36 Gα49B1 double mutant and Gα49B1 norpA36 rdgA1 triple mutant photoreceptors. Responses to light are greatly reduced in norpA36 Gα49B1 double mutant photoreceptors compared to norpA36 single mutant photoreceptors.

Flies expressing Lpol\Ops1ninaE.PK in a ninaE17 Gα49B1 background show no response to light (measured using an ERG recording). Flies expressing Lpol\Ops1ninaE.T:Btau\1D4 in a ninaE17 Gα49B1 background show no response to light (measured using an ERG recording).

The small amplitude of quantum bumps in Gα49B1 photoreceptors (seen when ATP is present in the intracellular solution during recordings) can be restored to near a wild-type level if the flies are also mutant for rdgA3. The small amplitude of quantum bumps in Gα49B1 photoreceptors (seen when ATP is present in the intracellular solution during recordings) is not increased in size if the flies are also mutant for CdsA1.

The addition of rdgC306 to Gα49B1 flies undergo a dramatic and rapid loss of Deep Pseudopupils (DPPs) between days 4 and 6 of days of light exposure. This phenotype is partially rescued by the addition of Arr23, and enhanced (the numbers of DPPs start to reduce immediately on exposure to light) by the addition of Arr21. Gα49B1, Arr23 animals raised in normal light show normal ommatidial structure. Gα49B1, Arr21 animals raised in normal light show normal ommatidial structure. The light dependant retinal degeneration seen in Gα49B1, rdgC306 animals is strongly suppressed by Arr23.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Rescued by
Comments
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (16)
References (47)