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General Information
Symbol
Hsap\SNCAUAS.cFa
Species
H. sapiens
Name
Saccharomyces cerevisiae UAS construct a of Feany
FlyBase ID
FBal0104766
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-α-synuclein, UAS-α-syn, UAS-Hsap/SNCA.F, synWT, α-synWT, UAS-αSyn, UAS-Syn, UAS-hwt-SNCA, UASaSyn
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Carried in construct
Cytology
Nature of the lesion
Statement
Reference

UASt regulatory sequences drive expression of wild-type Hsap\SNCA.

Allele components
Product class / Tool use(s)
Encoded product / tool
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 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 2 )
 

Nicotinamide significantly improves the climbing ability of Hsap\SNCAScer\UAS.cFa flies.

Geldanamycin ( ChEBI:5292 ) protects against dopaminergic neuron loss in the DM clusters in Hsap\SNCAScer\UAS.cFa synucleinopathy model. Acts via Hsf, in Hsf4 flies, this protective function is lost.

Phenotypic Data
Phenotypic Class
Phenotype Manifest In

dopamine neuron & adult brain, with Scer\GAL4elav.PLu

Detailed Description
Statement
Reference

Expressing Hsap\SNCAUAS.cFa under the control of Scer\GAL4GMR.PS does not significantly affect the number of ommatidia.

Expressing Hsap\SNCAUAS.cFa under the control of Scer\GAL4elav.PU leads to a significant decrease in the number of dopaminergic neurons, but does not have a major effect in climbing activity, as compared to controls.

The expression of Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4elav-C155 leads to a significant and progressive decrease in adult locomotor capacity in negative geotaxis assays, and leads to a small but significant decrease in lifespan, as compared to controls.

Expression of Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4GMR.PU induces a rough eye phenotype in the adult eye.

Flies with expression of Hsap\SNCAScer\UAS.cFa driven by Scer\GAL4Ddc.PL have a decreased lifespan and impaired climbing ability. Flies with expression of Hsap\SNCAScer\UAS.cFa driven by Scer\GAL4GMR.PU have a rough eye phenotype.

The expression of Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4GMR.PU leads to a decrease in the number of ommatidia and disrupts the ommatidial array, as compared to controls. Expression under the control of Scer\GAL4Ddc.PL leads to a significant decrease in longevity and to a progressive decrease in adult locomotor ability in climbing assays, as compared to controls.

Expression of Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4Ddc.PL results in decreased median adult lifespan and rapid age-progressive decline in climbing ability.

Expression of Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4elav.PU results in loss of climbing ability in adult flies.

Adult flies expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4elav.PLu show decreased climbing ability and lower average activity compared to controls.

Adult flies expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4ple.PF fed with 1% glucose show a significantly lower survival rate and loss of dopaminergic neurons in the PPM1/2 cluster (other dopaminergic neuronal clusters - VUM, PAL, PPM3, PPL1 and PPL2 - are unaffected) but their locomotion (climbing ability) at 0-5 days post-eclosion is not impaired relative to wild-type.

Ectopic expression of Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4elav-C155 results in an increase in average amplitude of miniature excitatory junction potentials (mEJPs) at neuromuscular junctions of third instar larvae and the frequency distribution of mEJP amplitude sizes is significantly different compared to controls, the quantal content or the amplitude of evoked excitatory potentials (eEJPs) remains unchanged.

Ectopic expression of Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4elav-C155 results in an increased size of synaptic vesicles and a shift in frequency distribution toward larger vesicles in both type 1b and 1s of neuromuscular junction boutons in third instar larvae compared to controls.

Ectopic expression of Hsap\SNCAScer\UAS.cFa under the control of either Scer\GAL4C164 or Scer\GAL4ple.PF results in a decrease in the distance travelled per unit of time by third instar larvae in a crawling assay compared to controls.

Ectopic expression of Hsap\SNCAScer\UAS.cFa under the control of either Scer\GAL4C164 or Scer\GAL4ple.PF results in loss of dopaminergic neurons of the PPL1 cluster in the brain of adult flies.

Ectopic expression of Hsap\SNCAScer\UAS.cFa under the control Scer\GAL4GMR.PU results in loss of rhabdomeres in the eye of 30 day-old adults.

Ectopic expression of Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4elav-C155 results in defects in climbing behavior in adults of various ages (10, 20 and 30 day-old).

Ectopic expression of Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4ple.PF results in defects in climbing behavior in adults of various ages (10, 20 and 30 day-old).

Ectopic expression of Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4elav-C155 results in shortened lifespan of adult flies.

The expression of Hsap\SNCAUAS.cFa under the control of Scer\GAL4elav-C155 leads to loss of dopaminergic neurons, as assessed by the levels of TH, as compared to controls.

Flies expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4elav-C155 exhibit a mild decline in climbing ability from 4 weeks after eclosion, compared with control flies. Fewer dopaminergic neurons are seen compared with controls.

Expression of Hsap\SNCAScer\UAS.cFa in the developing eye under the control of Scer\GAL4GMR.PU induces a rough eye phenotype at 28[o]C.

Expression of Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4ple.PF does not lead to any significant difference in the number of dopaminergic neurons in newly eclosed adult males, but at 20 days post-eclosion, these flies show a significant decrease in neuron numbers in all dopaminergic neuron clusters.

Expression of Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4GMR.PS does not result in any obvious eye phenotype or reduction in life span, but do exhibit a progressive defect in climbing ability.

Expression of Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4ple.PF does not result in a loss of dopaminergic neurons in 55-day old flies.

Exposure to C.asiatica extract for 24 days delays the loss of climbing ability seen in flies expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4elav.PLu in a dose-dependent manner. C.asiatica extract has no effect on the climbing ability of control flies. C. asiatica extract also delays the loss of activity pattern seen in Hsap\SNCAScer\UAS.cFa-expressing flies, and a similar effect is seen when the flies are fed dopamine.

Flies expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4NP6510 show an accelerated age-dependent decline in locomotor performance in a startle-induced negative geotaxis (SING) assay compared to controls.

Flies expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4elav.PLu exhibit a decrease in lifespan and a decrease in physical activity, as compared to controls.

The climbing response in wild-type flies remains essentially unchanged over 21 days. From day 9 on, however, the response of flies expressing Scer\GAL4elav.PLu>Hsap\SNCAScer\UAS.cFa is significantly lower than that of controls. When the climbing assay is performed after 21 days of exposure to various doses of Eucalyptus citriodora leaf extract, it is found that the loss of climbing ability in transgenic flies is significantly delayed in a dose dependent manner.

Flies expressing Scer\GAL4elav.PLu>Hsap\SNCAScer\UAS.cFa show lower performance 12 days after eclosion in a climbing assay compared with wild-type. An alginate-curcumin nanocomposite supplement in the diet of transgenic flies results in a significant delay in the loss of their climbing ability.

Expression of Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4elav.PU results in a loss of climbing ability in adult flies. Addition of L-DOPA or GABA to the food of these flies restores their climbing ability. Addition of muscimol, a GABA[[A]] receptor agonist has no effect on the reduced climbing ability of Hsap\SNCAScer\UAS.cFa flies. However, the GABA[[B]] receptor agonist baclofen does repair climbing ability.

Expression of Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4GMR.PS results in a rough eye phenotype.

Expression of Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4elav-C155 leads to toxicity and ultrastructural abnormalities in ommatidia.

Expression of Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4ple.PF causes a significant reduction in the number of dopaminergic neurons.

Expression of Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4unspecified causes decreased motility and premature death.

Flies over-expressing Hsap\SNCAIPScer\UAS.cHa under the control of Scer\GAL4unspecified display abnormalities in their electroretinograms (ERG). The amplitude of the sustained component of the photoreceptor potential (PP) and the overshoot (OS) are affected. Treatment with L-Dopa/carbidopa reverts the effect of the over-expression of the transgene.

20 day old adults expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4ple.PF show significant loss of dopaminergic (DA) neurons in both the dorsomedial, posteriomedial and dorsolateral 1 clusters (loss of DA neurons is not see in 10 day old adults of this genotype).

20 to 30 day old adults expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4GMR.PU show a neurodegenerative phenotype in the eyes, with less photoreceptor cells than normal and disruption of the ommatidia.

Adults expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4ple.PF do not show noticeable defects in climbing ability until 20 days after eclosion.

Lewy body-like Hsap\SNCA positive inclusions are clearly observed in the brains of 10 and 20 day old adults expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4ple.PF and the number and size of the inclusions gradually increases with age.

Expression of Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL430Y leads to age-progressive short-term (60 min) memory loss (measured by assessing courtship behavior in adult males).

In 1-day, 5-day and 10-day old flies expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4elav.PU, the number of dopaminergic neurons in the dorsomedial clusters is not significantly different from the number in controls. However, at 20 days, there is a marked loss of neurons.

Scer\GAL4GMR.PU-mediated expression of Hsap\SNCAScer\UAS.cFa causes mild adult-onset retinal degeneration manifested by disruption of the normal arrangement of ommatidia.

Expression of Hsap\SNCA driven by Scer\GAL4GMR.PF causes the degeneration of rhabdomeres in the eyes of Drosophila.

Transgenic flies expressing Hsap\SNCA driven by Scer\GAL4elav-C155 show an age-dependent decline in negative geotactic locomotory response starting from 27 days after eclosion.

Expression of Hsap\SNCAScer\UAS.cFa driven by Scer\GAL4Ddc.PL results in a significant reduction in the number of dorsomedial cluster 1 dopaminergic neurons in the brain.

Flies expressing Hsap\SNCAScer\UAS.cFa in dopaminergic neurons under the control of Scer\GAL4ple.PF develop an age-dependent neurodegeneration that can be detected at day 15, and continuously increases with age leading to a loss of about 20% of all dopaminergic neurons after 40 days. No loss of dopaminergic neurons is seen in age-matched wild type flies.

Expression of Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4ple.PF does not suppress the hypoxia-induced dopaminergic neuron degeneration seen in control flies.

Flies expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4Ddc.PL show a progressive decrease in climbing ability over time. This defect can be significantly improved by feeding with nicotinamide.

Flies expressing Hsap\SNCAScer\UAS.cFa under the control of either Scer\GAL4Ddc.PL or Scer\GAL4elav.PU prematurely develop age-related climbing defects. Lifespan is unaffected.

The retinas of three day old flies expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4GMR.PF are intact, whereas premature deterioration is observed at 30 days old.

20 day old flies expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4elav.PLu show a marked loss of dopamine neurons in the dorsomedial cluster. If the flies are fed either AK-1 or AGK2 for the first 20 days of adult life, a dose-dependent rescue of this loss of neuron phenotype is seen.

Expression of Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4elav.PU results in age-progressive loss of dopaminergic neurons in the adult brain and aged adult flies (20 days) display abnormal neuronal inclusions in the lamina cell cortex and neuropil.

Expression of Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4ple.PF results in loss of dopaminergic neurons in aged brains.

Flies expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4elav.PU show a progressive loss of dorsomedial dopamine neurons in the brain. This neurodegeneration can be rescued by feeding the flies sodium butyrate or SAHA.

1 day old flies expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4elav.PU have a normal number of dorsomedial dopaminergic neurons, while 20 day old flies show a substantial loss of these neurons compared to wild type.

Adults expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4GMR.PF show mild retinal degeneration with vacuolisation and disruption of the normal arrangement of ommatidia.

When Hsap\SNCAScer\UAS.cFa is driven by Scer\GAL4GMR.PF premature degeneration of the ommatidial architecture is seen in thirty day old flies. The external morphology of the eyes in unaffected. When Hsap\SNCAScer\UAS.cFa is driven by Scer\GAL4Ddc.PL mutant animals prematurely lose their climbing ability.

20 day old flies expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4Ddc.PL have a 50% reduction in the number of dopaminergic neurons in the dorsomedial clusters of the brain.

20 day old (but not 1 day old) flies expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4Ddc.PL show marked loss of neurons in the dorsomedial (DM) dopaminergic clusters. Neuron loss is more variable in the dorsolateral (DL)-1 dopaminergic clusters, ranging from no loss of neurons to as much as 50% of neurons being lost. Inclusions are present in the dopaminergic neurons of flies expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4Ddc.PL. These inclusions increase in size and number with age. Most inclusions are in the DL-1 and DL-2 clusters and they are only rarely seen in the DM clusters.

Flies expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4elav.PLu show a marked, age-dependent loss of dorsomedial dopaminergic neurons. Hsap\SNCA inclusions in the brain (detected by immunostaining) are seen in aged flies (the inclusions are first seen at 20-30 days of age). Most neuronal cytoplasmic inclusions are single, round and regular, although a few are more irregular. Neuritic Hsap\SNCA inclusions are also present in the brain and consist of both thread- and grain-like inclusions. Locomotor behaviour is grossly preserved in young flies expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4elav.PLu. These flies initially climb as well as wild-type flies, but over time they show a premature loss of climbing ability compared to control flies. Flies expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4GMR.PF show retinal degeneration that is detectable by 10 days, and marked at 30 days after eclosion.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference
NOT Enhanced by
Suppressed by
Statement
Reference
NOT suppressed by
Enhancer of
Statement
Reference
Other
Phenotype Manifest In
Enhanced by
Statement
Reference
NOT Enhanced by
Suppressed by
Statement
Reference

Hsap\SNCAUAS.cFa, Scer\GAL4GMR.PU has eye | heat sensitive phenotype, suppressible by Nedd4UAS.Tag:MYC, Scer\GAL4GMR.PU

NOT suppressed by
Enhancer of
Other
Additional Comments
Genetic Interactions
Statement
Reference

The co-expression of BuffyScer\UAS.cQa suppresses the ommatidial defects (i.e ommatidial number and ommatidial array organization ) induced by the expression of either Pi3K59FKK107602 or Atg6GD11647 under the control of Scer\GAL4GMR.PU.

The co-expression of BuffyScer\UAS.cQa respectively enhances and suppresses the Atg6GD11647- Pi3K59FKK107602-induced (expression driven by Scer\GAL4Ddc.PL) decreased longevity and progressive decrease in adult locomotion.

Xenogenetic Interactions
Statement
Reference

Co-expressing Hsap\SNCAUAS.cFa with Hsap\DNAJC13wt.UAS.Tag:MYC under the control of Scer\GAL4GMR.PS does not significantly affect the number of ommatidia.

Co-expressing Hsap\SNCAUAS.cFa with Hsap\DNAJC13N855S.UAS.Tag:MYC, but not with Hsap\DNAJC13wt.UAS.Tag:MYC, under the control of Scer\GAL4elav.PU leads to a significant, age-dependent decrease in climbing activity.

The co-expression of Hsap\SNCAScer\UAS.cFa with either Glo1KK109109 or TpiGD10138 under the control of Scer\GAL4elav-C155 leads to a significant and progressive decrease in adult locomotor capacity (in negative geotaxis assays) and a significant decrease in lifespan; these are more severe than the respective single expressions, with the exception that the decreased lifespan induced by the Hsap\SNCAScer\UAS.cFa, TpiGD10138 co-expression is only more severe than the TpiGD10138 single expression condition.

The rough eye phenotype characteristic for adult flies expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4GMR.PU is restored by co-expression of Usp8HMS01898 and worsened further by co-expression of Vps28GD7696.

Co-expression of BuffydsRNA.Scer\UAS enhances shortened lifespan in flies with expression of Hsap\SNCAScer\UAS.cFa driven by Scer\GAL4Ddc.PL. Co-expression of BuffyScer\UAS.cQa suppresses shortened lifespan and impaired climbing ability in flies with expression of Hsap\SNCAScer\UAS.cFa driven by Scer\GAL4Ddc.PL.

Co-expression of BuffydsRNA.Scer\UAS enhances the rough eye phenotype seen in flies with expression of Hsap\SNCAScer\UAS.cFa driven by Scer\GAL4GMR.PU. Co-expression of BuffyScer\UAS.cQa suppresses the rough eye phenotype seen in flies with expression of Hsap\SNCAScer\UAS.cFa driven by Scer\GAL4GMR.PU.

The co-expression of either Hsap\SNCAScer\UAS.cFa and Pi3K59FKK107602 or Hsap\SNCAScer\UAS.cFa and Atg6GD11647 under the control of Scer\GAL4GMR.PU, leads to a decrease in the number of ommatidia and consequent disruption of the ommatidial array, both of which are more severe than upon each single expression conditions.

The decreased longevity, but not the progressive decrease in adult locomotion, induced by the expression of Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4Ddc.PL is enhanced by the co-expression of either Pi3K59FKK107602 or Atg6GD11647.

The reduced adult lifespan and poor climbing ability characteristic for adult flies expressing Hsap\SNCAScer\UAS.cFa (with the Scer\GAL4Ddc.PL driver) as well as the morphological eye defects and ommatidial disarray (using the Scer\GAL4GMR.PF driver) are significantly improved by co-expression of DebclJF02429 RNAi, while co-expression of DebclScer\UAS.T:Ivir\HA1 further worsens the phenotypes.

Co-expression of Rab11Scer\UAS.T:Avic\GFP-EGFP suppresses increased mEJP and eEJP amplitudes and increased quantal content as well as increased synaptic vesicle size at boutons at the NMJs in third instar larvae expressing Hsap\SNCAScer\UAS.cFa driven by Scer\GAL4elav-C155

The defective crawling behavior (decrease in distance travelled per unit of time) characteristic for third instar larvae expressing Hsap\SNCAScer\UAS.cFa under the control of either Scer\GAL4C164 or Scer\GAL4ple.PF can be suppressed by co-expression of Rab11Scer\UAS.T:Avic\GFP-EGFP using the Scer\GAL4C164 driver and partially suppressed when the Scer\GAL4ple.PF driver is used.

The loss of dopaminergic PPL1 neurons in the adult brain characteristic for flies expressing Hsap\SNCAScer\UAS.cFa under the control of either Scer\GAL4elav-C155 or Scer\GAL4ple.PF can be reversed by co-expression of Rab11Scer\UAS.T:Avic\GFP-EGFP using either of the two drivers.

The decrease in the number of rhabdomeres in the adult eye observed in flies expressing Hsap\SNCAScer\UAS.cFa under the control Scer\GAL4GMR.PU can be partially restored by co-expression of Rab11Scer\UAS.T:Avic\GFP-EGFP.

The defects in climbing behavior seen in adult flies or various ages (10, 20 and 30 day-old) expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4elav-C155 can be suppressed by co-expression of Rab11Scer\UAS.T:Avic\GFP-EGFP.

The defects in climbing behavior seen in adult flies or various ages (10, 20 and 30 day-old) expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4ple.PF are suppressed by co-expression of Rab11Scer\UAS.T:Avic\GFP-EGFP in 30 day-old flies only.

The shortened lifespan characteristic for adult flies expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4elav-C155 can be reversed by co-expression of Rab11Scer\UAS.T:Avic\GFP-EGFP.

Expression of Gba1aGD6246 enhances the reduction in climbing activity and loss of dopaminergic neurons seen in flies expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4elav-C155.

The eyes of flies co-expressing Hsap\SNCAScer\UAS.cFa and Gba1aGD6246 under the control of Scer\GAL4GMR.PS exhibit retinal thinning. No thinning is seen when either transgene is expressed alone.

Expression of GalGD936 enhances the reduction in climbing activity seen in flies expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4elav-C155.

Co-expression of Nedd4Scer\UAS.T:Hsap\MYC suppresses the rough eye phenotype induced by expression of Hsap\SNCAScer\UAS.cFa in the developing eye under the control of Scer\GAL4GMR.PU.

Knockdown of Nedd4, through expression of Nedd4GD5146 does not affect the rough eye phenotype induced by Hsap\SNCAScer\UAS.cFa in the developing eye under the control of Scer\GAL4GMR.PU.

Co-expression of Nedd4Scer\UAS.T:Hsap\MYC prevents the climbing deficit associated with neuronal Hsap\SNCAScer\UAS.cFa expression (both constructs under the control of Scer\GAL4elav.PU.

Knockdown of Nedd4, through expression of Nedd4GD5146, significantly worsens the climbing deficits found upon Hsap\SNCAScer\UAS.cFa expression (both constructs under the control of Scer\GAL4elav.PU).

Knockdown of Nedd4, through expression of Nedd4GD5146, combined with expression of Hsap\SNCAScer\UAS.cFa, in the nervous system (under the control of Scer\GAL4elav.PU) leads to a significant reduction in the number of ple-positive neurons in the dorsomedial cluster when compared to controls.

Co-expression of Nedd4Scer\UAS.T:Hsap\MYC prevents Hsap\SNCAScer\UAS.cFa-induced dopaminergic cell loss.

Expression of Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4ple.PF in chico1/+ mutants does not lead to any significant difference in the number of dopaminergic neurons in newly eclosed adult males, but chico1/+ suppresses the dopaminergic neuron loss seen in 20 day old flies expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4ple.PF.

Expression of Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4ple.PF in PgiEY09730/+ mutants does not lead to any significant difference in the number of dopaminergic neurons in newly eclosed adult males, but these flies show enhanced dopaminergic neuron loss seen at 20 days old as compared to either PgiEY09730/+ mutants or flies expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4ple.PF.

Co-expression of Vps35GD11710 and Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4GMR.PS leads to a small reduction in size of each ommatidium along with loss of interommatidial bristles, as compared to controls; and leads to a more severe progressive climbing defect, as compared to expression of either single allele alone.

The rough eye phenotype caused by expression of Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4GMR.PS is suppressed by co-expression of Hsap\CRYABScer\UAS.T:Ivir\HA1.

Co-expression of Hsap\SNCAIPScer\UAS.cHa and Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4elav-C155 suppresses the ommatidium phenotype resulting from the expression of either transgene alone.

Co-expression of Hsap\SNCAIPScer\UAS.cHa and Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4ple.PF increases the number of dopaminergic neurons compared with wild-type or the expression-phenotype of either transgene alone.

Flies co-expressing Hsap\SNCAIPScer\UAS.cHa and Hsap\SNCAScer\UAS.cFa via Scer\GAL4unspecified show reduction in age-associated motility and mortality very similar to that of wild-type controls.

HDAC6KO enhances the loss of dopaminergic (DA) neurons caused by expression of Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4ple.PF; the neuron degeneration phenotype is apparent at 10 days after eclosion in the double mutant flies, and 20 days after eclosion it is more severe than that seen in the Hsap\SNCAScer\UAS.cFa, Scer\GAL4ple.PF single mutants.

HDAC6KO enhances the retinal degeneration phenotype seen in adults expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4GMR.PU.

Co-expression of HDAC6Scer\UAS.cDa suppresses the retinal degeneration phenotype seen in adults expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4GMR.PU.

HDAC6KO enhances the climbing ability defect caused by expression of Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4ple.PF; defects are seen 10 days after eclosion in the double mutant flies (defects are not seen until 20 days after eclosion in Hsap\SNCAScer\UAS.cFa, Scer\GAL4ple.PF single mutants) and the defects at 20 days after eclosion are more severe in the double mutants.

HDAC6KO decreases the number of Lewy body-like Hsap\SNCA positive inclusions seen in the brains of adults expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4ple.PF such that no inclusions are seen in 10 day old flies and the number of inclusions seen in 20 days old flies is reduced.

Coexpression of sharkScer\UAS.cFa significantly rescues the neurotoxicity of Scer\GAL4elav.PU-mediated Hsap\SNCAScer\UAS.cFa expression.

Co-expression of Hsap\UBCScer\UAS.T:Ivir\HA driven by Scer\GAL4GMR.PF significantly suppresses the neurodegenerative process induced by Hsap\SNCAScer\UAS.cFa.

Co-expression of Hsap\UBCK48.Scer\UAS.T:Ivir\HA driven by Scer\GAL4GMR.PF significantly suppresses the neurodegenerative process induced by Hsap\SNCAScer\UAS.cFa.

Co-expression of Hsap\UBCK63R.Scer\UAS.T:Ivir\HA driven by Scer\GAL4GMR.PF significantly suppresses the neurodegenerative process induced by Hsap\SNCAScer\UAS.cFa.

Co-expression of Hsap\UBCK48R.Scer\UAS.T:Ivir\HA driven by Scer\GAL4GMR.PF does not suppresses the neurodegenerative process induced by Hsap\SNCAScer\UAS.cFa.

Co-expression of Hsap\UBCK63.Scer\UAS.T:Ivir\HA driven by Scer\GAL4GMR.PF does not suppresses the neurodegenerative process induced by Hsap\SNCAScer\UAS.cFa.

Co-expression of Hsap\UBCScer\UAS.T:Ivir\HA driven by Scer\GAL4elav-C155 in transgenic flies significantly suppresses the Hsap\SNCAScer\UAS.cFa-induced motor impairment.

Co-expression of Hsap\UBCK48.Scer\UAS.T:Ivir\HA driven by Scer\GAL4elav-C155 in transgenic flies significantly suppresses the Hsap\SNCAScer\UAS.cFa-induced motor impairment.

Co-expression of Hsap\UBCK63R.Scer\UAS.T:Ivir\HA driven by Scer\GAL4elav-C155 in transgenic flies significantly suppresses the Hsap\SNCAScer\UAS.cFa-induced motor impairment.

Co-expression of Hsap\UBCK48R.Scer\UAS.T:Ivir\HA driven by Scer\GAL4elav-C155 in transgenic flies does not suppresses the Hsap\SNCAScer\UAS.cFa-induced motor impairment.

Co-expression of Hsap\UBCK63.Scer\UAS.T:Ivir\HA driven by Scer\GAL4elav-C155 in transgenic flies does not suppresses the Hsap\SNCAScer\UAS.cFa-induced motor impairment.

Co-expression of Hsap\UBCScer\UAS.T:Ivir\HA driven by Scer\GAL4Ddc.PL suppresses the Hsap\SNCAScer\UAS.cFa-induced loss of dorsomedial cluster 1 dopaminergic neurons in the brain.

Expression of Pink1Scer\UAS.cTa completely suppresses the premature loss of climbing ability seen when Hsap\SNCAScer\UAS.cFa is expressed under the control of Scer\GAL4Ddc.PL. The lifespan of these flies is similar to controls.

Expression of Hsap\SNCAScer\UAS.cFa enhances the rough eye phenotype seen in Scer\GAL4GMR.PF/+ flies at 29[o]C. Approximately 50% of the eye area contains fused or enlarged ommatidia. Co-expression of Pink1Scer\UAS.cTa suppresses this phenotype, returning the proportion of eye fusion to the level seen when Scer\GAL4GMR.PF is expressed alone. The retinal deterioration seen in 30 day old flies is suppressed.

The loss of dopaminergic neurons that is seen in the brains of flies expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4ple.PF is suppressed by co-expression of Mmus\Rab1Scer\UAS.cCa.

Sin3A08269 rescues the progressive loss of dorsomedial dopamine neurons in the brain seen in flies expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4elav.PU.

Co-expression of Gprk2Scer\UAS.cCb enhances the loss of dorsomedial dopaminergic neurons which is seen in adults expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4elav.PU, with cell loss being seen in 10 day old double mutant flies.

Co-expression of Gprk2Scer\UAS.cCb and Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4GMR.PF results in marked cell loss in the retina as early as 10 days of age.

The reduction in the number of dopaminergic neurons in the dorsomedial clusters of the brain seen in 20 day old flies expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4Ddc.PL is suppressed by coexpression of Hsap\PARK2Scer\UAS.cYa.

The loss of dorsomedial dopaminergic neurons seen in 20 day old flies expressing Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4Ddc.PL is suppressed by co-expression of Hsap\HSPA1LScer\UAS.cWa, although there is no change in the number, morphology or distribution of inclusions seen in the dopaminergic neurons. Co-expression of Hsc70-4K71S.Scer\UAS accelerates the loss of dopaminergic neurons caused by expression of Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4Ddc.PL; neuronal loss is apparent in 1 day old flies expressing both Hsc70-4K71S.Scer\UAS and Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4Ddc.PL whereas neuronal loss in flies overexpressing only Hsap\SNCAScer\UAS.cFa under the control of Scer\GAL4Ddc.PL occurs by 10 to 20 days.

Complementation and Rescue Data
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Synonyms and Secondary IDs (7)
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Symbol Synonym
Hsap\SNCAScer\UAS.cFa
Hsap\SNCAUAS.cFa
Name Synonyms
Saccharomyces cerevisiae UAS construct a of Feany
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    References (61)