FB2024_03 , released June 25, 2024
Allele: Hsap\SNCAUAS.cTa
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General Information
Symbol
Hsap\SNCAUAS.cTa
Species
H. sapiens
Name
Saccharomyces cerevisiae UAS construct a of Trinh
FlyBase ID
FBal0277666
Feature type
allele
Associated gene
Hsap\SNCA
Associated Insertion(s)
Carried in Construct
P{UAS-Hsap\SNCA.T}
Also Known As
UAS-Syn, UAS-α-Syn, UAS-α-Synuclein LP2
Key Links
Transgenic product class
wild_type
(Trinh et al., 2008)
Mutagen
Nature of the Allele
Transgenic product class
wild_type
(Trinh et al., 2008)
Mutagen
in vitro construct
(Trinh et al., 2008)
Progenitor genotype
Carried in construct
P{UAS-Hsap\SNCA.T}
Cytology
Description

UASt regulatory sequences are cloned upstream of Hsap\SNCA coding sequences.

(Trinh et al., 2008)
Allele components
Component
Use(s)
Regulatory region(s)
UASt
Encoded product / tool
Hsap\SNCA
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
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 ( 1 )
      Modifiers Based on Experimental Evidence ( 1 )
      Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
       
      Disease-implicated variant(s)
       
      Phenotypic Data
      Phenotypic Class
      Phenotype Manifest In
      Detailed Description
      Statement
      Reference

      Expression of two copies of Hsap\SNCAScer\UAS.cTa under the control of Scer\GAL4ple.PF leads to a small, non-significant decrease in the number of dopaminergic neurons in the PPL1 cluster in adults, and leads to decreased lifespan, but does not cause climbing defects, heat stress recovery defects, or bang sensitivity, as compared to controls.

      (Davis et al., 2016)

      Expression of Hsap\SNCAScer\UAS.cTa under the control of Scer\GAL4ple.PF results in dopaminergic cell loss in the dorsolateral cluster.

      (Roy and Jackson, 2014)

      Third instar larvae expressing Hsap\SNCAScer\UAS.cTa in dopaminergic neurons under the control of Scer\GAL4ple.PF have significantly slower locomotion compared to wild type.

      The brains of third instar larvae expressing Hsap\SNCAScer\UAS.cTa under the control of Scer\GAL4ple.PF have a decreased number of dopaminergic neurons in each of the three clusters (dorsomedial, dorsolateral 1 and dorsolateral 2). The phenotype is age-dependent; the number of DA neurons in first instar larvae is similar to wild type.

      (Varga et al., 2014)

      Expression of Hsap\SNCAScer\UAS.cTa under the control of Scer\GAL4elav.PLu or Scer\GAL4ple.PF causes age-dependent defects in the negative geotaxis response (i.e. the innate tendency to walk upwards after being tapped to the bottom of their containing vial).

      Brains from aged Hsap\SNCAScer\UAS.cTa-expressing flies exhibit an average loss of 1.5-2 neurons per PPL1 cluster, relative to age-matched controls.

      (Barone et al., 2011)

      One-day old flies expressing two copies of Hsap\SNCAScer\UAS.cTa under the control of two copies of Scer\GAL4ple.PF do not exhibit a loss of ple-positive neurons, relative to controls. In contrast, 20-day old flies carrying two copies of Hsap\SNCAScer\UAS.cTa and two copies of Scer\GAL4ple.PF exhibit a statistically significant reduction in the number of ple-positive neurons in the protocerebral posterior lateral 1 (PPL1) cluster, relative to wild-type controls. Neuronal loss is not detected in flies bearing one or two copies of Hsap\SNCAScer\UAS.cTa and Scer\GAL4elav.PLu at 20 or more days of age.

      Feeding sulforaphane or allyl disulfide to flies expressing Hsap\SNCAScer\UAS.cTa under the control of Scer\GAL4ple.PF suppresses DA neuron loss.

      (Trinh et al., 2008)
      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Enhanced by
      Suppressed by
      NOT suppressed by
      Enhancer of
      Other
      Phenotype Manifest In
      Enhanced by
      Suppressed by
      NOT suppressed by
      Enhancer of
      Other
      Additional Comments
      Genetic Interactions
      Statement
      Reference
      Xenogenetic Interactions
      Statement
      Reference

      Df(3R)GBA1ΔTT/Df(3R)GBA1ΔTT enhances the dopaminergic neuron loss to a significant level, leads to climbing defects and reduced recovery after heat-induced paralysis, and enhances the reduced survival, but does not lead to bang sensitivity in flies expressing two copies of Hsap\SNCAScer\UAS.cTa under the control of Scer\GAL4ple.PF.

      (Davis et al., 2016)

      Expression of Hsap\SNCAScer\UAS.cTa under the control of Scer\GAL4GMR.PS enhances the rough eye phenotype seen in flies expressing Hsap\MAPTGMR.Ex.PJ, with the phenotype extending farther posteriorly. Eyes of animals co-expressing Hsap\SNCAScer\UAS.cTa are more flattened than those expressing Hsap\MAPTGMR.Ex.PJ alone.

      Expression of Hsap\SNCAScer\UAS.cTa enhances the appreciable increase in cell death (cleaved caspase activity) posterior to the morphogenetic furrow seen in flies expressing Hsap\MAPTScer\UAS.wt under the control of Scer\GAL4GMR.PS.

      Expression of Hsap\SNCAScer\UAS.cTa enhances the severe motor deficits seen in flies expressing Hsap\MAPTScer\UAS.wt in post-mitotic neurons under the control of Scer\GAL4elav-C155.

      Expression of Hsap\SNCAScer\UAS.cTa enhances the proportion of abnormal boutons in the neuromuscular junctions of larvae expressing Hsap\MAPTScer\UAS.wt under the control of Scer\GAL4RapGAP1-OK6.

      Expression of Hsap\MAPTScer\UAS.wt enhances the dopaminergic cell loss seen in the dorsolateral cluster of flies expressing Hsap\SNCAScer\UAS.cTa under the control of Scer\GAL4ple.PF results in dopaminergic cell loss in the dorsolateral cluster.

      Flies co-expressing Hsap\SNCAScer\UAS.cTa and Hsap\MAPTGMR.Ex.PJ under the control of Scer\GAL4GMR.PS show highly disorganised actin bundles.

      Expression of Hsap\SNCAScer\UAS.cTa enhances the extent of the microtubule shaft disorganisation seen in the retinas of flies expressing Hsap\MAPTGMR.Ex.PJ.

      Expression of Hsap\SNCAScer\UAS.cTa enhances the increase in segmental nerve axonal aggregates seen in larvae expressing Hsap\MAPTScer\UAS.wt under the control of Scer\GAL4VGlut-OK371.

      (Roy and Jackson, 2014)

      Co-expression of cncScer\UAS.cSa with Hsap\SNCAScer\UAS.cTa (specifically at 2-5 days after eclosion), under the control of Scer\GAL4ple.PF, prevents the deficit in locomotor performance induced by Hsap\SNCAScer\UAS.cTa expression.

      Expression of cncScer\UAS.cSa at 25[o]C 2-5 days after eclosion has no effect on the age-associated decline in negative geotaxis found in flies expressing Hsap\SNCAScer\UAS.cTa under the control of Scer\GAL4ple.PF.

      Flies expressing Hsap\SNCAScer\UAS.cTa under the control of Scer\GAL4ple.PF in a Keap1EY5/+ background display locomotor activity similar to that of wild-type flies, indicating that the Keap1EY5/+ background suppresses the age-dependent decay in negative geotaxis response found in Hsap\SNCAScer\UAS.cTa-expressing flies.

      A Keap1EY5/+ background, the neuron loss experienced in PPL1 clusters upon expression of Hsap\SNCAScer\UAS.cTa under the control of Scer\GAL4ple.PF is restored to wild-type levels.

      Flies co-expressing Hsap\SNCAScer\UAS.cTa and Keap1dsRNA.Scer\UAS under the control of Scer\GAL4ple.PF display locomotor activity similar to that of wild-type flies, indicating suppression of the age-dependent negative geotaxis response found in Hsap\SNCAScer\UAS.cTa-expressing flies.

      Co-expression of maf-SScer\UAS.T:Ivir\HA1 with Hsap\SNCAScer\UAS.cTa, both under the control of Scer\GAL4ple.PF, suppresses the age-dependent defects in negative geotaxis.

      Co-expression of maf-SScer\UAS.T:Ivir\HA1 in flies expressing Hsap\SNCAScer\UAS.cTa under the control of Scer\GAL4ple.PF, does not affect the number of PPL1 neurons in either young or old flies, but is sufficient to rescue the Hsap\SNCA-induced neurotoxicity in old flies.

      (Barone et al., 2011)

      A Df(3L)H99 background suppresses the neuronal loss seen upon expression of multiple copies of Hsap\SNCAScer\UAS.cTa under the control of Scer\GAL4ple.PF.

      A GstS1M26 mutant background enhances the DA neuron loss found in flies expressing Hsap\SNCAScer\UAS.cTa under the control of Scer\GAL4ple.PF.

      Co-expression of GstS1Scer\UAS.P\T.cWa fully suppresses the neuronal loss observed in 2-day old flies expressing two copies of Hsap\SNCAScer\UAS.cTa under the control of two copies of Scer\GAL4ple.PF.

      The decreased Gclm activity in GclmL0580 homozygotes is found to significantly enhance the DA neuron loss induced by expression of Hsap\SNCAScer\UAS.cTa under the control of Scer\GAL4ple.PF.

      Expression of GclmScer\UAS.cOa completely rescues the neuronal loss induced by Hsap\SNCAScer\UAS.cTa expression in 20- and 30-day old flies.

      (Trinh et al., 2008)
      Complementation and Rescue Data
      Comments
      Images (0)
      Mutant
      Wild-type
      Stocks (1)
      Notes on Origin
      Discoverer
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (3)
      Reported As
      Symbol Synonym
      Hsap\SNCAScer\UAS.cTa
      Hsap\SNCAUAS.cTa
      Name Synonyms
      Saccharomyces cerevisiae UAS construct a of Trinh
      Secondary FlyBase IDs
        References (10)