A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Allele Dmel\VGlutScer\UAS.cDa

General Information
SymbolDmel\VGlutScer\UAS.cDaSpeciesD. melanogaster
NameSaccharomyces cerevisiae UAS construct a of DanielsFlyBase IDFBal0175767
Feature typealleleAssociated geneDmel\VGlut
Allele class
Mutagenin vitro construct - regulatory fusion
hide Recent Updates
Description
What does this section display?
This section contains items that were added to this record for each release. It currently only tracks new links between this FlyBase report and other FlyBase data classes (e.g. genes, references, stocks) or controlled vocabulary terms (e.g. GO, anatomy terms).
What does this section not display?
This section does not currently display links that were removed or gene model changes.
Update Feed
Click the icon below to subscribe to this FlyBase record and receive updates automatically through your feed reader.
FB2013_03
FB2013_02
All updates Click here to see a list of all updates to this record from FB2010_08 and on.
hide Nature of the Allele
Allele class
Mutagen
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
Construct: Scer\UAS regulatory sequences drive expression of a VGlut cDNA.
Carried in construct
Cytology
hide Phenotypic Data
hide Phenotypic Class
hide Phenotype Manifest In
hide Detailed Description
Statement
Reference
Intracellular voltage recordings in muscles of animals overexpressing VGlut[Scer\UAS.cDa] driven by Scer\GAL4[VGlut.PD] or Scer\GAL4[BG380] reveal large spontaneous events in motoneurons. Driving VGlut[Scer\UAS.cDa] withe the strong Scer\GAL4[BG380] driver results in death during larval stages. Driving VGlut[Scer\UAS.cDa] with Scer\GAL4[VGlut.PD] results in lethality within the first few weeks of adulthood. Flies overexpressing VGlut[Scer\UAS.cDa] driven by Scer\GAL4[VGlut.PD] are uncoordinated and cannot fly. VGlut[Scer\UAS.cDa]-overexpressing flies display progressive motor defects manifesting in impaired negative geotaxis.
Expression of VGlut[Scer\UAS.cDa] in post-mitotic neurons under the control of Scer\GAL4[elav-C155] causes a significant increase in average mEPSP amplitude. There is also a homeostatic decrease in presynaptic quantal content in these mutants.
Males expressing VGlutScer\UAS.cDa under the control of Scer\GAL4αTub84B.PL show high levels of homosexual courtship, which includes all aspects of sexual behaviour (including singing, genital licking and attempted copulation). Occasionally, the males attempt copulation with inappropriate body reions, such as the head. Males expressing VGlutScer\UAS.cDa under the control of Scer\GAL4NP0225 show a significant amount of homosexual behaviour, although less than seen when the Scer\GAL4αTub84B.PL driver is used. Expression of VGlutScer\UAS.cDa under the control of Scer\GAL4Mef2.247 has no affect on the courtship behaviour of males.
Expression of VGlutScer\UAS.cDa under the control of Scer\GAL4BG380 results in an increase of about 60% in the mean mEJP amplitude recorded from the muscle of the larval neuromuscular junction compared to wild type. The amplitude of the entire population of mEJP events seems to be increased in size, with the median amplitude increasing by 35% compared to wild type. There is a small increase in mEJP frequency. Larvae expressing VGlutScer\UAS.cDa under the control of Scer\GAL4BG380 show no significant difference in the amplitude of evoked EJPs recorded from the muscle of the larval neuromuscular junction compared to wild type. Quantal content is decreased relative to wild type. Larvae expressing VGlutScer\UAS.cDa under the control of Scer\GAL4BG380 show an increase in synaptic vesicle size (assayed at the neuromuscular junction of the type Ib motorneuron that innervates muscles 6 and 7) compared to wild type; a 14% increase in mean vesicle outer diameter and a median increase in vesicle outer diameter of 10% is seen.
hide External Data
Linkouts
hide Interactions
hide Phenotypic Class
hideNOT Enhanced by
Statement
Reference
hideNOT suppressed by
Statement
Reference
hide Phenotype Manifest In
hideNOT Enhanced by
Statement
Reference
hideNOT suppressed by
Statement
Reference
hide Additional Comments
hide Genetic Interactions
Statement
Reference
Expression of VGlut[Scer\UAS.cDa] and gsb[491.dsRNA.Scer\UAS] in post-mitotic neurons under the control of Scer\GAL4[elav-C155] causes a significant increase in average mEPSP amplitude. There is also a homeostatic decrease in presynaptic quantal content in these mutants.
hide Xenogenetic Interactions
Statement
Reference
hide Complementation & Rescue Data
Rescues
Comments
Expression of VGlut[Scer\UAS.cDa] in motor neurons under the control of Scer\GAL4[BG380] rescues the decrease in mEJP frequency in VGlut[1]/Df(2L)VGlut[2] mutant synapses. These larvae exhibit a slight increase in quantal size compared to controls.
hide Stocks ( 0 )
hide Notes on Origin
Discoverer
hide External Crossreferences & Linkouts
Other Crossreferences
Linkouts
hide Synonyms & Secondary IDs ( 2 )
Reported As
Symbol Synonym
VGlutScer\UAS.cDa
 
Name Synonym
Saccharomyces cerevisiae UAS construct a of Daniels
Secondary FlyBase IDs
hide References ( 5 )
Research paper
Daniels et al., 2011, Neurobiol. Disease 41(2): 415--420
Increased vesicular glutamate transporter expression causes excitotoxic neurodegeneration. [FBrf0212635]
Marie et al., 2010, J. Neurosci. 30(24): 8071--8082
Synaptic homeostasis is consolidated by the cell fate gene gooseberry, a Drosophila pax3/7 homolog. [FBrf0211066]
Grosjean et al., 2008, Nat. Neurosci. 11(1): 54--61
A glial amino-acid transporter controls synapse strength and courtship in Drosophila. [FBrf0201004]
Daniels et al., 2006, Neuron 49(1): 11--16
A single vesicular glutamate transporter is sufficient to fill a synaptic vesicle. [FBrf0191312]
Daniels et al., 2004, J. Neurosci. 24(46): 10466--10474
Increased expression of the Drosophila vesicular glutamate transporter leads to excess glutamate release and a compensatory decrease in quantal content. [FBrf0180418]