FlyBase Allele Report: Dmel\Gαs[B19]

General Information

Symbol

Dmel\Gαs^B19

Species

D. melanogaster

Name

FlyBase ID

FBal0095722

Feature type

allele

Associated gene

Dmel\Gαs

Associated Insertion(s)

Carried in Construct

Also Known As

dgs^B19

Key Links

Genomic Maps

JBrowse

Allele class

hypomorphic allele - genetic evidence

Mutagen

ethyl methanesulfonate

Nature of the Allele

Allele class

hypomorphic allele - genetic evidence

(Wolfgang et al., 2004)

Mutagen

ethyl methanesulfonate

(Wolfgang et al., 2001, Wolfgang et al., 1999)

Progenitor genotype

Cytology

Description

Nucleotide substitution: A1117T. Amino acid replacement: I373F.

(Wolfgang et al., 2001)

Single amino acid substitution.

(Wolfgang et al., 1999)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

point_mutation

2R:23,946,706..23,946,706 [+]

Nucleotide change:

A23946706T

Reported nucleotide change:

A1117T

Amino acid change:

Reported amino acid change:

I373F

(Wolfgang et al., 2001)

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

Phenotype Manifest In

bouton

(Wolfgang et al., 2004)

bouton (with Df(2R)or-BR11)

(Wolfgang et al., 2004)

embryonic/larval fat body

(Wolfgang et al., 2001)

pupa

(Wolfgang et al., 2001)

synapse

(Wolfgang et al., 2004)

Detailed Description

Statement

Reference

Gαs^B19 mutant flies show resistance to V. cholerae infection compared to controls.

(Blow et al., 2005)

In homozygous mutant larvae, the overall pattern of innervation is normal. In second instar homozygous larvae, the extent of synaptic branching is slightly reduced, but the number of synaptic boutons is not significantly different to controls. However, the number of synaptic boutons is significantly decreased in the wandering stage third instar larvae. Bouton numbers are further decreased in G-sα60A^B19/Df(2R)or-BR11 larvae. Decreased numbers of boutons are associated with significant decrease in the extent of synaptic arborization in both homozygous and hemizygous larvae. Muscle and neuronal development is normal in these mutants. When nerves in mutant larvae are stimulated at 0.3 Hz, the average amplitudes of synaptic currents are normal. When the stimulus frequency is increased to 109 Hz for 50s, the amplitude of synaptic currents does not increase either during or immediately after tetanic stimulation.

(Wolfgang et al., 2004)

G-sα60A^B19 mutant third instar larvae show reduced facilitation during tetanus and lack of post-tetanic potentiation.

(Hou et al., 2003)

6% of homozygous embryos die. Homozygous, transheterozygous and hemizygous larvae survive for varying lengths of time, with a very few becoming pharate adults that never eclose. The mutant larvae are lethargic, grow more slowly and are thinner and more transparent due to reduced amounts of fat body compared to heterozygous siblings. Pupation of homozygous larvae is delayed by at least 1 day in uncrowded conditions, compared to control larvae. The pupae are deformed due to incomplete shortening of the body during pupariation and the larval mouthhooks are often not withdrawn into the pupal case. 30% of homozygous larvae pupate, compared to 11% of hemizygotes. Homozygous pharate adults have normal external morphology, but when removed from the pupal case are immobile. Third instar homozygous and hemizygous larvae crawl shorter distances than heterozygous controls. Some larvae crawl in continuous circles, backwards or on their backs for extended periods of time, behaviours that are not seen in wild type or heterozygotes. The larvae appear not to be attracted to yeast granules. Ovaries of females carrying homozygous germ-line clones appear normal. 97% of G-sα60A^B19/G-sα60A^R19 embryos derived from females carrying G-sα60A^B19 homozygous germ-line clones do not have cuticle defects.

(Wolfgang et al., 2001)

Animals die during the larval and pupal stages and never eclose. Development is delayed and larvae have behavioural abnormalities.

(Wolfgang et al., 1999)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Phenotype Manifest In

NOT Enhanced by

Statement

Reference

Gαs^B19 has phenotype, non-enhanceable by Adcy1^rut-1

(Wolfgang et al., 2004)

NOT suppressed by

Statement

Reference

Gαs^B19 has phenotype, non-suppressible by Adcy1^rut-1

(Wolfgang et al., 2004)

Gαs^B19 has bouton phenotype, non-suppressible by Gαi^UAS.cLa/Scer\GAL4^elav.PLu

(Wolfgang et al., 2004)

Gαs^B19 has synapse phenotype, non-suppressible by Gαi^UAS.cLa/Scer\GAL4^elav.PLu

(Wolfgang et al., 2004)

Enhancer of

Statement

Reference

Gαs^B19/G-salpha60A[+] is an enhancer of scutellar bristle | increased number phenotype of Ssdp^L7

(Bronstein et al., 2010)

Gαs^B19/G-salpha60A[+] is an enhancer of wing margin phenotype of Bx²

(Bronstein et al., 2010)

NOT Enhancer of

Statement

Reference

Gαs^B19 is a non-enhancer of phenotype of Adcy1^rut-1

(Wolfgang et al., 2004)

Suppressor of

Statement

Reference

Gαs^B19/G-salpha60A[+] is a suppressor of scutellar bristle | increased number phenotype of Chi^e5.5

(Bronstein et al., 2010)

Gαs^B19 is a suppressor of synapse | ectopic phenotype of Sh²¹, eag¹

(Wolfgang et al., 2004)

Gαs^B19 is a suppressor of synapse | ectopic phenotype of Fas2^e86

(Wolfgang et al., 2004)

Gαs^B19 is a suppressor of synapse | ectopic phenotype of Pde4^dnc-1

(Wolfgang et al., 2004)

NOT Suppressor of

Statement

Reference

Gαs^B19 is a non-suppressor of phenotype of Adcy1^rut-1

(Wolfgang et al., 2004)

Additional Comments

Genetic Interactions

Statement

Reference

eag¹. Sh²¹ mutants exhibit a synaptic phenotype. The addition of G-sα60A^B19 suppresses this phenotype. The addition of G-sα60A^B19 suppresses the synaptic over-growth phenotype seen in dnc¹ mutants. The addition of rut¹ to G-sα60A^B19 larvae has no effect on synapse formation.