FlyBase Allele Report: Dmel\Gαq[1]

General Information

Symbol

Dmel\Gαq¹

Species

D. melanogaster

Name

FlyBase ID

FBal0052412

Feature type

allele

Associated gene

Dmel\Gαq

Associated Insertion(s)

Carried in Construct

Also Known As

dgq¹, Gα_q¹, G_αq¹, Gα49B¹, Gaq¹, Gαq1, Gq¹

Key Links

Genomic Maps

JBrowse

Allele class

hypomorphic allele - genetic evidence

Mutagen

ethyl methanesulfonate

Nature of the Allele

Allele class

hypomorphic allele - genetic evidence

(Meyer et al., 2006, Scott et al., 1995)

Mutagen

ethyl methanesulfonate

(Scott et al., 1995)

Progenitor genotype

Cytology

Description

G to A nucleotide substitution (location 2R:12617455 , release 6 genome). This should disrupt the splice acceptor site of the Gαq RD and RJ isoforms.

(Chen, 2021.7.2)

G to A nucleotide substitution (coordinate 1910 of GenBank accession M58016.1; FlyBase curator comment: this corresponds to 2R:12617455 on the release 6 genome, as described in FBrf0249416). This maps to a splice acceptor site (at the intron 3-exon 4 boundary of the isoform represented by M58016.1). Loss of this splice acceptor site results in the use of a cryptic splice site 9 nucleotides downstream during transcription, causing an in-frame deletion of 3 codons (encompassing amino acid residues 154-156 of the isoform represented by GenBank protein accession AAA28460.1).

(Scott et al., 1995)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

point_mutation

2R:12,617,455..12,617,455 [+]

Nucleotide change:

G12617455A

Comment:

Splice acceptor mutation expected to disrupt splicing of the exon unique to the RD and RJ isoforms.

(Chen, 2021.7.2)

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

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 )

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

abnormal behavior | recessive

(Scott et al., 1995)

abnormal chemosensory behavior | adult stage

(Kwon et al., 2010)

abnormal immune response

(Ha et al., 2009)

abnormal neuroanatomy | third instar larval stage

(Park et al., 2017)

abnormal neurophysiology

(Knox et al., 2003, Hardie et al., 2002)

abnormal neurophysiology (with Gαq⁹⁶¹)

(Hu et al., 2012)

abnormal neurophysiology | adult stage

(Cao et al., 2018, Kwon et al., 2010)

abnormal neurophysiology | adult stage (with Gαq^V303D)

(Cao et al., 2018)

abnormal thermotaxis

(Kwon et al., 2008)

abnormal thermotaxis | third instar larval stage

(Sokabe et al., 2016)

abnormal visual behavior | recessive

(Scott and Zuker, 1998, Scott et al., 1995)

short lived | nutrition conditional

(Ha et al., 2009)

viable (with Gαq^221c)

(Kain et al., 2008)

viable (with Gαq¹³⁷⁰)

(Kain et al., 2008)

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.

(Cao et al., 2018)

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.

(Park et al., 2017)

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.

(Sokabe et al., 2016)

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.

(Zhang et al., 2013)

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.

(Hu et al., 2012)

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

(Kwon et al., 2010)

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.

(Kwon et al., 2010)

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.

(Ha et al., 2009)

Gα49B¹/Gα49B^221c and Gα49B¹/Gα49B¹³⁷⁰ flies do not show any defects in electroantennogram recordings.

(Kain et al., 2008)

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).

(Kwon et al., 2008)

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

(Ni et al., 2008)

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

(Meyer et al., 2006)

Endocytosis of ninaE is normal in Gα49B¹ photoreceptors.

(Satoh and Ready, 2005)

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.

(Iakhine et al., 2004)

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

(Lee and Montell, 2004)

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

(Knox et al., 2003)

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

(Kosloff et al., 2003)

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.

(Hardie et al., 2002)

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.

(Agam et al., 2000)

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

(Kiselev et al., 2000)

Linolenic acid can activate light sensitive channels in mutant photoreceptors.

(Chyb et al., 1999)

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

(Scott and Zuker, 1998)

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

(Vinos et al., 1997)

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.

(Scott et al., 1995)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

Gαq¹ has abnormal neurophysiology phenotype, suppressible by Gβ76C¹

(Elia et al., 2005)

Gαq¹ has abnormal neurophysiology phenotype, suppressible by rdgA³

(Hardie et al., 2002)

NOT suppressed by

Statement

Reference

Gαq¹ has abnormal thermotaxis phenotype, non-suppressible by TrpA1¹

(Kwon et al., 2008)

Gαq¹ has abnormal neurophysiology phenotype, non-suppressible by Cds¹

(Hardie et al., 2002)

NOT Enhancer of

Statement

Reference

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

(Park et al., 2017)

Suppressor of

Statement

Reference

Gαq¹ is a suppressor of abnormal neurophysiology phenotype of Camta^tes-2

(Han et al., 2006)

Gαq¹ is a suppressor of abnormal neurophysiology phenotype of Gβ76C¹

(Elia et al., 2005)

Arr2⁵/Gαq¹ is a suppressor of increased cell death phenotype of ninaE^pp100

(Iakhine et al., 2004)

Gαq¹ is a suppressor | partially of increased cell death phenotype of ninaE^pp100

(Iakhine et al., 2004)

Phenotype Manifest In

Enhanced by

Statement

Reference

Gαq¹, rdgC³⁰⁶ has ommatidium phenotype, enhanceable by Arr2¹

(Kiselev et al., 2000)

Suppressed by

Statement

Reference

Gαq¹ has photoreceptor neuron phenotype, suppressible by rdgA³

(Hardie et al., 2002)

Gαq¹, rdgC³⁰⁶ has ommatidium phenotype, suppressible by Arr2³

(Kiselev et al., 2000)

NOT suppressed by

Statement

Reference

Gαq¹ has photoreceptor neuron phenotype, non-suppressible by Cds¹

(Hardie et al., 2002)

NOT Enhancer of

Statement

Reference

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

(Park et al., 2017)

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

(Park et al., 2017)

Suppressor of

Statement

Reference

Gαq¹ is a suppressor of rhabdomere phenotype of tadr¹

(Ni et al., 2008)

Gαq¹ is a suppressor of eye photoreceptor cell phenotype of Camta^tes-2

(Han et al., 2006)

Gαq¹ is a suppressor of rhabdomere phenotype of rdgA³

(Georgiev et al., 2005)

Gαq¹ is a suppressor | partially of retina phenotype of ninaE^pp100

(Iakhine et al., 2004)

Arr2⁵/Gαq¹ is a suppressor of retina phenotype of ninaE^pp100

(Iakhine et al., 2004)

Gαq¹ is a suppressor of ommatidium phenotype of Arr2³

(Kiselev et al., 2000)

Other

Statement

Reference

Gαq¹, rdgC³⁰⁶ has ommatidium phenotype

(Kiselev et al., 2000)

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.

(Kwon et al., 2008)

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

(Ni et al., 2008)

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

(Han et al., 2006)

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

(Elia et al., 2005)

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

(Georgiev et al., 2005)

Gα49B¹; ninaE^pp100 double mutant flies show a significant rescue of the ninaE^pp100 retinal degeneration phenotype to the levels of Gα49B¹ single mutants.

Gα49B¹; Arr2⁵, ninaE^pp100 triple mutants show a suppression of the retinal degeneration phenotypes seen in ninaE^pp100 single mutants. The triple mutants exhibit only very minor rhabdomeric abnormalities after 40 days.

(Iakhine et al., 2004)

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.

(Hardie et al., 2003)

Flies expressing Lpol\Ops1^ninaE.PK in a ninaE¹⁷ Gα49B¹ background show no response to light (measured using an ERG recording). Flies expressing Lpol\Ops1^{ninaE.T:Btau\1D4} in a ninaE¹⁷ Gα49B¹ background show no response to light (measured using an ERG recording).

(Knox et al., 2003)

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.

(Hardie et al., 2002)

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.

(Kiselev et al., 2000)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescued by

Gαq¹ is rescued by Gαq^1.hs

(Scott et al., 1995)

Comments

Images (0)

Mutant

Wild-type

Stocks (1)

Bloomington

42257

cn¹ Gαq¹

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (16)

Reported As

Symbol Synonym

Dgq¹

(Vinos et al., 1997)

G_αq¹

(Leung et al., 2020, Vasiliauskas et al., 2011, Ni et al., 2008, Knox et al., 2003)

Gaq¹

(Elia et al., 2005, Hardie et al., 2002)

Gq¹

(Omelchenko et al., 2022, Thakur et al., 2016)

Gqα¹

(Yasin et al., 2017)

Gα1¹

(Baumann, 2004)

Gα49B¹

(Sokabe et al., 2016, Kwon et al., 2008, Meyer et al., 2008, Meyer et al., 2006)

Gα_q¹

(Cao et al., 2018, Park et al., 2017, Hu et al., 2012, Elsaesser et al., 2010, Yao and Carlson, 2010)

Gα¹_q

(Cao et al., 2018)

Gαq1

(Agam et al., 2000, Cook et al., 2000)

Gαq¹

(Gu et al., 2022, Gu et al., 2020, Kamalesh et al., 2017, Lee et al., 2013, Elsaesser et al., 2010, Ha et al., 2009, Han et al., 2006, Elia et al., 2005, Hardie et al., 2004, Hardie et al., 2003, Chyb et al., 1999, Scott and Zuker, 1998, Scott et al., 1997, Scott et al., 1995)

dGq¹

(Kamalesh et al., 2017, Zhang et al., 2013, Georgiev et al., 2005)

dGqα¹

(Kwon et al., 2010, Kwon et al., 2010)

dgq¹

(Satoh et al., 2010, Kain et al., 2008, Sanxaridis et al., 2007, Satoh and Ready, 2005, Iakhine et al., 2004, Kiselev et al., 2000)

dgqα1¹

(Iakhine et al., 2001)

g_qα¹

(Rosenbaum et al., 2011)

Name Synonyms

Secondary FlyBase IDs

References (50)

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