Allele Dmel\Gαs^B19

General Information
Symbol	Dmel\Gαs^B19	Species	D. melanogaster
Name		FlyBase ID	FBal0095722
Feature type	allele	Associated gene	Dmel\Gαs
Also Known As	dgs^B19, B19

Allele class	hypomorphic allele - genetic evidence
Mutagen	ethyl methanesulfonate
Recent Updates
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FB2013_03
FB2013_02
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Nature of the Allele
Allele class	hypomorphic allele - genetic evidence (Wolfgang et al., 2004)
Mutagen	ethyl methanesulfonate (Wolfgang et al., 1999, Wolfgang et al., 2001)
Mutations Mapped to the Genome

Type Location Additional Notes References
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype
Nature of the lesion	Statement Reference Nucleotide substitution: A1117T. Amino acid replacement: I373F. (Wolfgang et al., 2001) Single amino acid substitution. (Wolfgang et al., 1999)
Cytology
Phenotypic Data
Phenotypic Class
	behavior defective \| recessive (Wolfgang et al., 1999) developmental rate defective \| recessive (Wolfgang et al., 2001) hypoactive \| larval stage \| recessive (Wolfgang et al., 2001) lethal \| recessive (Wolfgang et al., 2001, Wolfgang et al., 1999) locomotor behavior defective \| larval stage \| recessive (Wolfgang et al., 2001) neurophysiology defective (Hou et al., 2003, Wolfgang et al., 2004)
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 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 the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
NOT Enhanced by
Statement Reference Gαs^B19 has phenotype, non-enhanceable by rut¹ (Wolfgang et al., 2004)
NOT suppressed by
Statement Reference Gαs^B19 has bouton phenotype, non-suppressible by Gαi^Scer\UAS.cLa/Scer\GAL4^elav.PLu (Wolfgang et al., 2004) Gαs^B19 has phenotype, non-suppressible by rut¹ (Wolfgang et al., 2004) Gαs^B19 has synapse phenotype, non-suppressible by Gαi^Scer\UAS.cLa/Scer\GAL4^elav.PLu (Wolfgang et al., 2004)
Enhancer of
Statement Reference Gαs^B19/G-salpha60A[+] is an enhancer of scutellar bristle \| supernumerary 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 rut¹ (Wolfgang et al., 2004)
Suppressor of
Statement Reference Gαs^B19/G-salpha60A[+] is a suppressor of scutellar bristle \| supernumerary phenotype of Chi^e5.5 (Bronstein et al., 2010) Gαs^B19 is a suppressor of synapse \| ectopic phenotype of dnc¹ (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 Sh²¹, eag¹ (Wolfgang et al., 2004)
NOT Suppressor of
Statement Reference Gαs^B19 is a non-suppressor of phenotype of rut¹ (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. (Wolfgang et al., 2004)
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Rescued by	Gαs^B19 is rescued by Gαs^+t10 (Wolfgang et al., 2004, Wolfgang et al., 2001) Gαs^B19 is rescued by Gαs^Scer\UAS.cCa/Scer\GAL4^B185 (Wolfgang et al., 2004)
Partially rescued by	Gαs^B19 is partially rescued by Gαs^Scer\UAS.cCa/Scer\GAL4^C57 (Wolfgang et al., 2004) Gαs^B19 is partially rescued by Gαs^Scer\UAS.cCa/Scer\GAL4^elav.PLu (Wolfgang et al., 2004) Gαs^B19 is partially rescued by Gαs^Scer\UAS.cCa/Scer\GAL4^Mhc.PW (Wolfgang et al., 2004) Gαs^B19 is partially rescued by Scer\GAL4^futsch-C380/Gαs^Scer\UAS.cCa (Wolfgang et al., 2004)
Comments
Stocks ( 1 )
Bloomington	6339 P{neoFRT}42D bw¹ Gαs^B19/SM6b, P{eve-lacZ8.0}SB1
Notes on Origin
Discoverer

External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 7 )
Reported As
Symbol Synonym	B19 (Wolfgang et al., 1999, Aravamudan and Broadie, 2003) dgs^B19 (Hou et al., 2003, Wolfgang et al., 2004, Wolfgang et al., 2003, Wolfgang et al., 2001) Gsa^B19 (Hannan et al., 2006) Gsalpha60A^B19 (Bronstein et al., 2010) G-sα60A^B19 Gsα^B19 (Hannan et al., 2006) Gαs^B19
Name Synonym
Secondary FlyBase IDs

References ( 9 )
Research paper	Bronstein et al., 2010, PLoS Genet. 6(8): e1001063 Transcriptional regulation by CHIP/LDB complexes. [FBrf0211594] Parrish et al., 2009, Neuron 63(6): 788--802 The microRNA bantam functions in epithelial cells to regulate scaling growth of dendrite arbors in drosophila sensory neurons. [FBrf0208858] Hannan et al., 2006, Hum. Mol. Genet. 15(7): 1087--1098 Effect of neurofibromatosis type I mutations on a novel pathway for adenylyl cyclase activation requiring neurofibromin and Ras. [FBrf0190827] Wolfgang et al., 2004, Dev. Biol. 268(2): 295--311 Signaling through Gs alpha is required for the growth and function of neuromuscular synapses in Drosophila. [FBrf0174523] Aravamudan and Broadie, 2003, J. Neurobiol. 54(3): 417--438 Synaptic Drosophila UNC-13 is regulated by antagonistic G-protein pathways via a proteasome-dependent degradation mechanism. [FBrf0155886] Hou et al., 2003, J. Neurosci. 23(13): 5897--5905 Presynaptic impairment of synaptic transmission in Drosophila embryos lacking Gs(alpha). [FBrf0160617] Wolfgang et al., 2001, Genetics 158(3): 1189--1201 Genetic analysis of the Drosophila Gs gene. [FBrf0137254]
Abstract	Wolfgang et al., 2003, A. Dros. Res. Conf. 44: 724A Is PKA downstream of Gsalpha signaling during larval synaptic growth? [FBrf0154384] Wolfgang et al., 1999, A. Dros. Res. Conf. 40: 1 Mutations in the subunit of a heterotrimeric G-protein. [FBrf0107493]

Allele Dmel\GαsB19

Allele Dmel\Gαs^B19