Allele Hsap\SNCA^Scer\UAS.cTa

General Information
Symbol	Hsap\SNCA^Scer\UAS.cTa	Species	H. sapiens
Name		FlyBase ID	FBal0277666
Feature type	allele	Associated gene	Hsap\SNCA

Allele class
Mutagen	in vitro construct - regulatory fusion
Recent Updates
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FB2013_03
FB2013_02
All updates	Click here to see a list of all updates to this record from FB2010_08 and on.
Nature of the Allele
Allele class
Mutagen	in vitro construct - regulatory fusion (Trinh et al., 2008)
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 Scer\UAS regulatory sequences are cloned upstream of Hsap\SNCA coding sequences. (Trinh et al., 2008)
Carried in construct	P{UAS-Hsap\SNCA.T} (Trinh et al., 2008, Barone et al., 2011)
Cytology
Phenotypic Data
Phenotypic Class
	gravitaxis defective, with Scer\GAL4^ple.PF (Barone et al., 2011) locomotor behavior defective, with Scer\GAL4^ple.PF (Barone et al., 2011) neuroanatomy defective, with Scer\GAL4^ple.PF (Trinh et al., 2008, Barone et al., 2011)
Phenotype Manifest In
	dopaminergic neuron, with Scer\GAL4^ple.PF (Trinh et al., 2008) dopaminergic PPL1 neuron, with Scer\GAL4^ple.PF (Barone et al., 2011)
Detailed Description
	Statement Reference Expression of Hsap\SNCA[Scer\UAS.cTa] under the control of Scer\GAL4[elav.PLu] or Scer\GAL4[ple.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\SNCA[Scer\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\SNCA[Scer\UAS.cTa] under the control of two copies of Scer\GAL4[ple.PF] do not exhibit a loss of ple-positive neurons, relative to controls. In contrast, 20-day old flies carrying two copies of Hsap\SNCA[Scer\UAS.cTa] and two copies of Scer\GAL4[ple.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\SNCA[Scer\UAS.cTa] and Scer\GAL4[elav.PLu] at 20 or more days of age. Feeding sulforaphane or allyl disulfide to flies expressing Hsap\SNCA[Scer\UAS.cTa] under the control of Scer\GAL4[ple.PF] suppresses DA neuron loss. (Trinh et al., 2008)
External Data
Linkouts
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement Reference Hsap\SNCA^Scer\UAS.cTa, Scer\GAL4^ple.PF has neuroanatomy defective phenotype, enhanceable by Gclm^L0580 (Trinh et al., 2008) Hsap\SNCA^Scer\UAS.cTa, Scer\GAL4^ple.PF has neuroanatomy defective phenotype, enhanceable by GstS1^M26 (Trinh et al., 2008)
Suppressed by
Statement Reference Hsap\SNCA^Scer\UAS.cTa, Scer\GAL4^ple.PF has gravitaxis defective phenotype, suppressible by Keap1^{dsRNA.Scer\UAS}, Scer\GAL4^ple.PF (Barone et al., 2011) Hsap\SNCA^Scer\UAS.cTa, Scer\GAL4^ple.PF has gravitaxis defective phenotype, suppressible by Keap1^EY5/Keap1[+] (Barone et al., 2011) Hsap\SNCA^Scer\UAS.cTa, Scer\GAL4^ple.PF has gravitaxis defective phenotype, suppressible by maf-S^{Scer\UAS.T:Ivir\HA1}, Scer\GAL4^ple.PF (Barone et al., 2011) Hsap\SNCA^Scer\UAS.cTa, Scer\GAL4^ple.PF has locomotor behavior defective phenotype, suppressible by cnc^Scer\UAS.cSa, Scer\GAL4^ple.PF (Barone et al., 2011) Hsap\SNCA^Scer\UAS.cTa, Scer\GAL4^ple.PF has locomotor behavior defective phenotype, suppressible by Keap1^{dsRNA.Scer\UAS}, Scer\GAL4^ple.PF (Barone et al., 2011) Hsap\SNCA^Scer\UAS.cTa, Scer\GAL4^ple.PF has locomotor behavior defective phenotype, suppressible by Keap1^EY5/Keap1[+] (Barone et al., 2011) Hsap\SNCA^Scer\UAS.cTa, Scer\GAL4^ple.PF has locomotor behavior defective phenotype, suppressible by maf-S^{Scer\UAS.T:Ivir\HA1}, Scer\GAL4^ple.PF (Barone et al., 2011) Hsap\SNCA^Scer\UAS.cTa, Scer\GAL4^ple.PF has neuroanatomy defective phenotype, suppressible by cnc^Scer\UAS.cSa, Scer\GAL4^ple.PF (Barone et al., 2011) Hsap\SNCA^Scer\UAS.cTa, Scer\GAL4^ple.PF has neuroanatomy defective phenotype, suppressible by Df(3L)H99 (Trinh et al., 2008) Hsap\SNCA^Scer\UAS.cTa, Scer\GAL4^ple.PF has neuroanatomy defective phenotype, suppressible by Gclm^Scer\UAS.cOa, Scer\GAL4^ple.PF (Trinh et al., 2008) Hsap\SNCA^Scer\UAS.cTa, Scer\GAL4^ple.PF has neuroanatomy defective phenotype, suppressible by GstS1^{Scer\UAS.P\T.cWa}, Scer\GAL4^ple.PF (Trinh et al., 2008) Hsap\SNCA^Scer\UAS.cTa, Scer\GAL4^ple.PF has neuroanatomy defective phenotype, suppressible by Keap1^{dsRNA.Scer\UAS}, Scer\GAL4^ple.PF (Barone et al., 2011) Hsap\SNCA^Scer\UAS.cTa, Scer\GAL4^ple.PF has neuroanatomy defective phenotype, suppressible by Keap1^EY5/Keap1[+] (Barone et al., 2011)
NOT suppressed by
Statement Reference Hsap\SNCA^Scer\UAS.cTa, Scer\GAL4^ple.PF has gravitaxis defective phenotype, non-suppressible by cnc^Scer\UAS.cSa, Scer\GAL4^ple.PF (Barone et al., 2011) Hsap\SNCA^Scer\UAS.cTa, Scer\GAL4^ple.PF has neuroanatomy defective phenotype, non-suppressible by maf-S^{Scer\UAS.T:Ivir\HA1}, Scer\GAL4^ple.PF (Barone et al., 2011)
Phenotype Manifest In
Enhanced by
Statement Reference Hsap\SNCA^Scer\UAS.cTa, Scer\GAL4^ple.PF has dopaminergic neuron phenotype, enhanceable by Gclm^L0580 (Trinh et al., 2008) Hsap\SNCA^Scer\UAS.cTa, Scer\GAL4^ple.PF has dopaminergic neuron phenotype, enhanceable by GstS1^M26 (Trinh et al., 2008)
Suppressed by
Statement Reference Hsap\SNCA^Scer\UAS.cTa, Scer\GAL4^ple.PF has dopaminergic neuron phenotype, suppressible by Df(3L)H99 (Trinh et al., 2008) Hsap\SNCA^Scer\UAS.cTa, Scer\GAL4^ple.PF has dopaminergic neuron phenotype, suppressible by Gclm^Scer\UAS.cOa, Scer\GAL4^ple.PF (Trinh et al., 2008) Hsap\SNCA^Scer\UAS.cTa, Scer\GAL4^ple.PF has dopaminergic neuron phenotype, suppressible by GstS1^{Scer\UAS.P\T.cWa}, Scer\GAL4^ple.PF (Trinh et al., 2008) Hsap\SNCA^Scer\UAS.cTa, Scer\GAL4^ple.PF has dopaminergic PPL1 neuron phenotype, suppressible by Keap1^EY5/Keap1[+] (Barone et al., 2011)
NOT suppressed by
Statement Reference Hsap\SNCA^Scer\UAS.cTa, Scer\GAL4^ple.PF has dopaminergic PPL1 neuron phenotype, non-suppressible by maf-S^{Scer\UAS.T:Ivir\HA1}, Scer\GAL4^ple.PF (Barone et al., 2011)
Additional Comments
Genetic Interactions
Statement Reference
Xenogenetic Interactions
Statement Reference Co-expression of cnc[Scer\UAS.cSa] with Hsap\SNCA[Scer\UAS.cTa] (specifically at 2-5 days after eclosion), under the control of Scer\GAL4[ple.PF], prevents the deficit in locomotor performance induced by Hsap\SNCA[Scer\UAS.cTa] expression. Expression of cnc[Scer\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\SNCA[Scer\UAS.cTa] under the control of Scer\GAL4[ple.PF]. Flies expressing Hsap\SNCA[Scer\UAS.cTa] under the control of Scer\GAL4[ple.PF] in a Keap1[EY5]/+ background display locomotor activity similar to that of wild-type flies, indicating that the Keap1[EY5]/+ background suppresses the age-dependent decay in negative geotaxis response found in Hsap\SNCA[Scer\UAS.cTa]-expressing flies. A Keap1[EY5]/+ background, the neuron loss experienced in PPL1 clusters upon expression of Hsap\SNCA[Scer\UAS.cTa] under the control of Scer\GAL4[ple.PF] is restored to wild-type levels. Flies co-expressing Hsap\SNCA[Scer\UAS.cTa] and Keap1[dsRNA.Scer\UAS] under the control of Scer\GAL4[ple.PF] display locomotor activity similar to that of wild-type flies, indicating suppression of the age-dependent negative geotaxis response found in Hsap\SNCA[Scer\UAS.cTa]-expressing flies. Co-expression of maf-S[Scer\UAS.T:Ivir\HA1] with Hsap\SNCA[Scer\UAS.cTa], both under the control of Scer\GAL4[ple.PF], suppresses the age-dependent defects in negative geotaxis. Co-expression of maf-S[Scer\UAS.T:Ivir\HA1] in flies expressing Hsap\SNCA[Scer\UAS.cTa] under the control of Scer\GAL4[ple.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\SNCA[Scer\UAS.cTa] under the control of Scer\GAL4[ple.PF]. A GstS1[M26] mutant background enhances the DA neuron loss found in flies expressing Hsap\SNCA[Scer\UAS.cTa] under the control of Scer\GAL4[ple.PF]. Co-expression of GstS1[Scer\UAS.P\T.cWa] fully suppresses the neuronal loss observed in 2-day old flies expressing two copies of Hsap\SNCA[Scer\UAS.cTa] under the control of two copies of Scer\GAL4[ple.PF]. The decreased Gclm activity in Gclm[L0580] homozygotes is found to significantly enhance the DA neuron loss induced by expression of Hsap\SNCA[Scer\UAS.cTa] under the control of Scer\GAL4[ple.PF]. Expression of Gclm[Scer\UAS.cOa] completely rescues the neuronal loss induced by Hsap\SNCA[Scer\UAS.cTa] expression in 20- and 30-day old flies. (Trinh et al., 2008)
Complementation & Rescue Data
Comments
Stocks ( 0 )

Notes on Origin
Discoverer

External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 1 )
Reported As
Symbol Synonym	Hsap\SNCA^Scer\UAS.cTa
Name Synonym
Secondary FlyBase IDs

References ( 2 )
Research paper	Barone et al., 2011, Dis. Model Mech. 4(5): 701--707 Genetic activation of Nrf2 signaling is sufficient to ameliorate neurodegenerative phenotypes in a Drosophila model of Parkinson's disease. [FBrf0215025] Trinh et al., 2008, J. Neurosci. 28(2): 465--472 Induction of the phase II detoxification pathway suppresses neuron loss in Drosophila models of Parkinson's disease. [FBrf0202781]

Allele Hsap\SNCAScer\UAS.cTa

Allele Hsap\SNCA^Scer\UAS.cTa