FlyBase Allele Report: Dmel\Gαs[Q215L.UAS]

General Information

Symbol

Dmel\Gαs^Q215L.UAS

Species

D. melanogaster

Name

FlyBase ID

FBal0058939

Feature type

allele

Associated gene

Dmel\Gαs

Associated Insertion(s)

Carried in Construct

P{UAS-Gαs.Q215L}

Also Known As

UAS-GαsQ215L

Key Links

Allele class

Mutagen

Nature of the Allele

Allele class

Mutagen

in vitro construct - regulatory fusion

(Wolfgang et al., 1996)

in vitro construct - amino acid replacement

(Connolly et al., 1996)

Mutations Mapped to the Genome

Type

Location

Additional Notes

References

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

Progenitor genotype

Gαs^UAS.cCa

(Connolly et al., 1996)

Carried in construct

P{UAS-Gαs.Q215L}

Cytology

Nature of the lesion

Statement

Reference

Amino acid replacement: Q215L. Impairs the GTPase activity resulting in a molecule that constitutively activates adenyl cyclase.

(Connolly et al., 1996)

An activated form of Gαs (contains the acid replacement: Q215L) is expressed under the control of UASt regulatory sequences.

(Wolfgang et al., 1996)

Allele components

Product class / Tool use(s)

Regulatory region(s)

UASt

binary expression system - regulatory region

Encoded product / tool

Gαs

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 circadian rhythm, with Scer\GAL4^P0.5.Pdf

(Dahdal et al., 2010)

abnormal learning, with Scer\GAL4^238Y

(Connolly et al., 1996)

abnormal learning, with Scer\GAL4^c309

(Connolly et al., 1996)

abnormal learning, with Scer\GAL4^c747

(Connolly et al., 1996)

abnormal learning, with Scer\GAL4^Tab2-201Y

(Connolly et al., 1996)

abnormal memory, with Scer\GAL4^c205

(Liu et al., 2006)

abnormal smell perception

(Xia and Tully, 2007)

abnormal smell perception, with Scer\GAL4^c309

(Xia and Tully, 2007)

abnormal smell perception, with Scer\GAL4^Tab2-201Y

(Xia and Tully, 2007)

increased cell death, with Scer\GAL4^en-e16E

(Kimura et al., 2004)

visible, with Scer\GAL4^30A

(Wolfgang et al., 1996)

visible, with Scer\GAL4^en-e16E

(Kimura et al., 2004)

visible, with Scer\GAL4^OK10

(Mistry et al., 2004)

Phenotype Manifest In

posterior scutellar bristle, with Scer\GAL4^OK10

(Mistry et al., 2004)

scutellum, with Scer\GAL4^OK10

(Mistry et al., 2004)

wing, with Scer\GAL4^30A

(Wolfgang et al., 1996)

wing, with Scer\GAL4^en-e16E

(Kimura et al., 2004)

wing, with Scer\GAL4^OK10

(Mistry et al., 2004)

wing | pharate adult stage, with Scer\GAL4^en-e16E

(Kimura et al., 2004)

Detailed Description

Statement

Reference

When driven by Scer\GAL4^elav-C155, overexpression of G-sα60A^{Q215L.Scer\UAS} does not alter neuromuscular junction morphology.

(Chen and Ganetzky, 2012)

Over 60% of flies expressing G-sα60A^{Q215L.Scer\UAS} under the control of Scer\GAL4^P0.5.Pdf in constant darkness are arrhythmic. While the remaining rhythmic flies exhibit normal periods, they are only weakly rhythmic, as shown by a lower rhythm power than control flies.

(Dahdal et al., 2010)

The response of the ab1C neuron to CO[[2]] is unaffected in animals expressing G-sα60A^{Q215L.Scer\UAS} under the control of Scer\GAL4^Gr21a.9.323.

The odour responses of the ab1A, ab2A and ab3A olfactory receptor neurons are unaffected in animals expressing G-sα60A^{Q215L.Scer\UAS} under the control of Scer\GAL4^{Orco.T:Hsim\VP16}.

Transient expression of G-sα60A^{Q215L.Scer\UAS} under the control of Scer\GAL4^hs.PU using heat shock results does not affect the spontaneous firing rate of the ab1C or ab3A ORNs compared to non-heat shocked controls.

(Yao and Carlson, 2010)

Expression of G-salpha60A^{Q215L.Scer\UAS} under the control of either Scer\GAL4^c309, Scer\GAL4²⁴⁷ (both drive expression in all lobes of the mushroom bodies) or Scer\GAL4^Tab2-201Y (in the γ-lobes) has no effect on spontaneous odor identity discrimination, nor conditioned odor intensity. However, conditioned odor identity discrimination is severely affected. This discrimination is abolished in a Scer\GAL80^ts.αTub84B background at 30[o]C.

(Xia and Tully, 2007)

Expression of G-sα60A^{Q215L.Scer\UAS} under the control of Scer\GAL4^c205 abolishes memory of the visual pattern element "elevation", but leaves memory of "contour orientation" intact. The abolition of memory of the "elevation" pattern parameter is also seen in flies in which G-sα60A^{Q215L.Scer\UAS} is expressed under the control of Scer\GAL4^c205 only in the adult (in this case Scer\GAL80^ts.αTub84B is used to block Scer\GAL4^c205 function throughout development, but it is then inactivated by raising adult flies at 30^oC, allowing Scer\GAL4^c205 to drive expression of G-sα60A^{Q215L.Scer\UAS} in the adults).

(Liu et al., 2006)

G-sα60A^{Q215L.Scer\UAS}; Scer\GAL4^en-e16E adults have blistered wings. There is precocious cell of wing blade cells in late stage pharate adults (G+; <3hrs before eclosion) of this genotype. However, wing cuticle structure is normal.

(Kimura et al., 2004)

Expression of G-sα60A^{Q215L.Scer\UAS} under the control of Scer\GAL4^OK10 results in wing blistering, shortening of the scutellum and crossing and inappropriate anterior orientation of the posterior scutellar bristles.

(Mistry et al., 2004)

When expression is driven by Scer\GAL4^238Y, Scer\GAL4^c309 or Scer\GAL4^c747 learning is abolished. When expression is driven by Scer\GAL4^Tab2-201Y learning is reduced by 50%. Olfactory responses to OCT and MCH are normal, as were responses to electroshock. When expression is driven by Scer\GAL4^Aph-4-c232 or Scer\GAL4^OK348 learning is not affected. When expression is driven by Scer\GAL4¹⁴⁰⁷ causes neither lethality nor overt behavioral defects.

(Connolly et al., 1996)

The dorsal and ventral surfaces of the wing do not adhere to each other and separate following emergence from the pupal case, producing wing blisters, when G-sα60A^{Q215L.Scer\UAS} is expressed using Scer\GAL4^30A or Scer\GAL4^OK10.

(Wolfgang et al., 1996)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

Gαs^Q215L.UAS, Scer\GAL4^P0.5.Pdf has abnormal circadian rhythm phenotype, suppressible by dnc^UAS.cCa, Scer\GAL4^P0.5.Pdf

(Dahdal et al., 2010)

Gαs^Q215L.UAS, Scer\GAL4^OK10 has visible phenotype, suppressible by Df(2L)osp29/+

(Mistry et al., 2004)

Gαs^Q215L.UAS, Scer\GAL4^OK10 has visible phenotype, suppressible by Df(3L)vin7/+

(Mistry et al., 2004)

Gαs^Q215L.UAS, Scer\GAL4^OK10 has visible phenotype, suppressible by gft[+]/Cul3^gft6

(Mistry et al., 2004)

Gαs^Q215L.UAS, Scer\GAL4^OK10 has visible phenotype, suppressible by gft[+]/Cul3^GR18

(Mistry et al., 2004)

Gαs^Q215L.UAS, Scer\GAL4^OK10 has visible phenotype, suppressible by gft[+]/Cul3^d577

(Mistry et al., 2004)

Gαs^Q215L.UAS, Scer\GAL4^OK10 has visible phenotype, suppressible | partially by Df(2L)wg-CX3/+

(Mistry et al., 2004)

Gαs^Q215L.UAS, Scer\GAL4^OK10 has visible phenotype, suppressible by gft[+]/Cul3⁰⁶⁴³⁰

(Mistry et al., 2004)

Gαs^Q215L.UAS, Scer\GAL4^OK10 has visible phenotype, suppressible by gft[+]/Cul3^gft1

(Mistry et al., 2004)

Gαs^Q215L.UAS, Scer\GAL4^OK10 has visible phenotype, suppressible by gft[+]/Cul3^gft2

(Mistry et al., 2004)

Gαs^Q215L.UAS, Scer\GAL4^OK10 has visible phenotype, suppressible by Cul3^gft4/gft[+]

(Mistry et al., 2004)

NOT suppressed by

Statement

Reference

Gαs^Q215L.UAS, Scer\GAL4^P0.5.Pdf has abnormal circadian rhythm phenotype, non-suppressible by Mmus\Cd8a^UAS.cLa.EGFP, Scer\GAL4^P0.5.Pdf

(Dahdal et al., 2010)

Other

Statement

Reference

Df(1)Exel9051/Df(1)Exel9051, Gαs^Q215L.UAS has abnormal neuroanatomy | third instar larval stage phenotype

(Chen and Ganetzky, 2012)

Phenotype Manifest In

Suppressed by

Statement

Reference

Gαs^Q215L.UAS, Scer\GAL4^OK10 has posterior scutellar bristle phenotype, suppressible by Df(2L)wg-CX3/+

(Mistry et al., 2004)

Gαs^Q215L.UAS, Scer\GAL4^OK10 has scutellum phenotype, suppressible by Df(2L)wg-CX3/+

(Mistry et al., 2004)

Gαs^Q215L.UAS, Scer\GAL4^OK10 has posterior scutellar bristle phenotype, suppressible by Df(3L)vin7/+

(Mistry et al., 2004)

Gαs^Q215L.UAS, Scer\GAL4^OK10 has scutellum phenotype, suppressible by Df(3L)vin7/+

(Mistry et al., 2004)

Gαs^Q215L.UAS, Scer\GAL4^OK10 has wing phenotype, suppressible by Df(3L)vin7/+

(Mistry et al., 2004)

Gαs^Q215L.UAS, Scer\GAL4^OK10 has wing phenotype, suppressible by gft[+]/Cul3⁰⁶⁴³⁰

(Mistry et al., 2004)

NOT suppressed by

Statement

Reference

Gαs^Q215L.UAS, Scer\GAL4^OK10 has wing phenotype, non-suppressible by Df(2L)wg-CX3/+

(Mistry et al., 2004)

Other

Statement

Reference

Df(1)Exel9051/Df(1)Exel9051, Gαs^Q215L.UAS has NMJ bouton | third instar larval stage phenotype

(Chen and Ganetzky, 2012)

Df(1)Exel9051/Df(1)Exel9051, Gαs^Q215L.UAS has embryonic/larval neuromuscular junction | third instar larval stage phenotype

(Chen and Ganetzky, 2012)

Additional Comments

Genetic Interactions

Statement

Reference

Overexpression of G-sα60A^{Q215L.Scer\UAS} completely suppresses the neuromuscular junction (NMJ) phenotype of Df(1)Exel9051/Y.

(Chen and Ganetzky, 2012)

The arrhythmicity caused by expression of G-sα60A^{Q215L.Scer\UAS} in LN[[v]] neurons under the control of Scer\GAL4^P0.5.Pdf in constant darkness is completely suppressed by co-expression of dnc^Scer\UAS.cCa. These flies also exhibit ~2hr shorter periods than flies expressing dnc^Scer\UAS.cCa alone.

(Dahdal et al., 2010)

Df(2L)wg-CX3/+ weakly suppresses the phenotype caused by expression of G-sα60A^{Q215L.Scer\UAS} under the control of Scer\GAL4^OK10; the scutellum and posterior scutellar bristles are normal, but the wings remain blistered. The phenotype caused by expression of G-sα60A^{Q215L.Scer\UAS} under the control of Scer\GAL4^OK10 is suppressed almost to wild type by either Df(2L)osp29/+ or Df(3L)vin7/+. gft⁰⁶⁴³⁰/+ moderately suppresses the phenotype caused by expression of G-sα60A^{Q215L.Scer\UAS} under the control of Scer\GAL4^OK10; wing blistering is reduced.

(Mistry et al., 2004)

Blisters are also produced when G-sα60A^{Q215L.Scer\UAS} is expressed using Scer\GAL4^30A in a vn¹ rho^ve-1 double mutant background. Reduction or elimination of protein kinase A activity has no effect on the phenotype generated when the G-sα60A pathway is activated in wing epithelial cells; wing duplications that contain blisters are formed when Pka-R1^BDK.Scer\UAS and G-sα60A^{Q215L.Scer\UAS} are co-expressed using Scer\GAL4^30A, and when G-sα60A^{Q215L.Scer\UAS} is expressed in a Pka-C1^H2 background using Scer\GAL4^OK10.

(Wolfgang et al., 1996)

Xenogenetic Interactions

Statement

Reference

The arrhythmicity caused by expression of G-sα60A^{Q215L.Scer\UAS} in LN[[v]] neurons under the control of Scer\GAL4^P0.5.Pdf in constant darkness is not suppressed by co-expression of Mmus\Cd8a^{Scer\UAS.T:Avic\GFP}.

(Dahdal et al., 2010)

Complementation and Rescue Data

Comments

Images (0)

Mutant

Wild-type

Stocks (2)

Bloomington

6490

w^*; P{UAS-Gαs.Q215L}16/TM3, Sb¹

Kyoto

108805