FlyBase Allele Report: Hsap\SNCA[A30P.UAS]

General Information

Symbol

Hsap\SNCA^A30P.UAS

Species

H. sapiens

Name

FlyBase ID

FBal0104768

Feature type

allele

Associated gene

Hsap\SNCA

Associated Insertion(s)

Carried in Construct

P{UAS-Hsap\SNCA.A30P}

Also Known As

UAS-A30P, UAS-SNCA^A30P, UAS-A30P α-synuclein, P{UAS-syn.A30P}, UAS-α-syn A30P, UAS-SNCA-A30P, UAS-αSynA30P, UAS-h[A30P]αSyn

Key Links

Transgenic product class

missense_variant

(Feany and Bender, 2000)

Mutagen

in vitro construct

Nature of the Allele

Transgenic product class

missense_variant

(Feany and Bender, 2000)

Mutagen

in vitro construct

(Feany and Bender, 2000)

Progenitor genotype

Carried in construct

P{UAS-Hsap\SNCA.A30P}

Cytology

Description

UASt regulatory sequences drive expression of the mutated A30P form of Hsap\SNCA (which is linked to a familial Parkinson's disease in humans).

(Feany and Bender, 2000)

Allele components

Component

Use(s)

Regulatory region(s)

UASt

binary expression system - regulatory region

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 )

Disease

Evidence

References

model of synucleinopathy

CEA

(Bayersdorfer et al., 2010)

model of Parkinson's disease

CEA

(Chen and Tully, 2018, Zhu et al., 2016, Jahromi et al., 2015, Jahromi et al., 2015, Kong et al., 2015, Chen et al., 2014, Chen et al., 2014, Riemensperger et al., 2013, Shaltiel-Karyo et al., 2012, Hernández-Vargas et al., 2011, Botella et al., 2008, Scherzer et al., 2003, Yang et al., 2003, Feany and Bender, 2000)

model of Parkinson's disease 1

CEC

(Huang et al., 2023, Golomidov et al., 2022, Liu et al., 2022, Xue et al., 2022, Cunningham et al., 2018)

CEA

(Dhanushkodi et al., 2023, Diaw et al., 2023, Ledahawsky et al., 2022, Rahmani et al., 2022, Dinh et al., 2021, Beaver et al., 2020, Yan et al., 2019, Coelho et al., 2018, Ito et al., 2017)

Modifiers Based on Experimental Evidence ( 1 )

Disease

Interaction

References

model of synucleinopathy

is ameliorated by ple^GD1181

(Bayersdorfer et al., 2010)

model of Parkinson's disease 1

is ameliorated by Jra^Jbz.UAS

(Liu et al., 2022)

is exacerbated by bsk^UAS.cBa

(Liu et al., 2022)

is ameliorated by Sfxn1-3^EY01545

(Ledahawsky et al., 2022)

is exacerbated by Tango14^GD481

(Xue et al., 2022)

is exacerbated by Tango14^JF01144

(Xue et al., 2022)

is exacerbated by anne^KK107621

(Dhanushkodi et al., 2023)

is ameliorated by Tip60^UAS.cUa

(Beaver et al., 2020)

is ameliorated by TP53INP^FENLL.UAS

(Dinh et al., 2021)

is ameliorated by TP53INP^long.UAS

(Dinh et al., 2021)

is ameliorated by egr^HMC03963

(Huang et al., 2023)

is exacerbated by Lamp1^11B

(Rahmani et al., 2022)

is exacerbated by Lamp1^6.1

(Rahmani et al., 2022)

is ameliorated by Lamp1^Tub.PR

(Rahmani et al., 2022)

is ameliorated by st^UAS.Venus

(Cunningham et al., 2018)

is ameliorated by Atg7^GD11671

(Yan et al., 2019)

is ameliorated by Ire1^GD3071

(Yan et al., 2019)

ameliorates Parkinson's disease

modeled by Hsap\SNCAIP^UAS.cHa

(Hernández-Vargas et al., 2011)

model of Parkinson's disease

is ameliorated by Hsap\SNCAIP^UAS.cHa

(Hernández-Vargas et al., 2011)

is ameliorated by Hsap\SOD1^UAS.cPa

(Botella et al., 2008)

exacerbates Kufor-Rakeb syndrome

modeled by anne^KK107621

(Dhanushkodi et al., 2023)

Comments on Models/Modifiers Based on Experimental Evidence ( 1 )

FlyBase curator comment: "Parkinson's disease 1" is associated with mutations in human SNCA.

(Cunningham et al., 2018)

Disease-implicated variant(s)

This allele represents a human variant implicated in disease.

(Feany and Bender, 2000)

SNCA:p.Ala30Pro

(FlyBase curators, 2019-)

Variants Synonym(s)

Associated human disease model(s)

Parkinson disease 1

External database links

ClinVar: SNCA_14008

Comments concerning this variant

Phenotypic Data

Phenotypic Class

abnormal courtship behavior, with Scer\GAL4^elav-C155

(Shaltiel-Karyo et al., 2012)

abnormal locomotor behavior, with Scer\GAL4^elav.PLu

(Feany and Bender, 2000)

abnormal locomotor behavior, with Scer\GAL4^ple.PF

(Bayersdorfer et al., 2010)

abnormal locomotor behavior | adult stage, with Scer\GAL4^Ddc.PL

(Riemensperger et al., 2013)

abnormal locomotor behavior | adult stage, with Scer\GAL4^elav-C155

(Jahromi et al., 2015, Riemensperger et al., 2013)

abnormal locomotor behavior | adult stage, with Scer\GAL4^GMR58E02

(Riemensperger et al., 2013)

abnormal locomotor behavior | adult stage, with Scer\GAL4^NP6510

(Riemensperger et al., 2013)

abnormal locomotor behavior | adult stage, with Scer\GAL4^ple.PF

(Botella et al., 2008)

abnormal locomotor behavior | adult stage | progressive, with Scer\GAL4^Ddc.PU

(Yan et al., 2019)

abnormal locomotor behavior | adult stage | progressive, with Scer\GAL4^elav.PU

(Chen and Tully, 2018, Chen et al., 2014)

abnormal locomotor behavior | adult stage | progressive, with Scer\GAL4^elav-C155

(Dinh et al., 2021, Issa et al., 2018, Kong et al., 2015)

abnormal locomotor behavior | adult stage | progressive, with Scer\GAL4^nSyb.PU

(Chen et al., 2014)

abnormal locomotor behavior | adult stage | progressive, with Scer\GAL4^ple.PF

(Cunningham et al., 2018)

abnormal locomotor behavior | progressive, with Scer\GAL4^elav-C155

(Shaltiel-Karyo et al., 2012)

abnormal locomotor rhythm | adult stage, with Scer\GAL4^Ddc.PL

(Dhanushkodi et al., 2023)

abnormal locomotor rhythm | adult stage, with Scer\GAL4^elav-C155

(Jahromi et al., 2015)

abnormal neuroanatomy, with Scer\GAL4^Ddc.PL

(Yang et al., 2003, Auluck et al., 2002)

abnormal neuroanatomy, with Scer\GAL4^ple.PF

(Bayersdorfer et al., 2010)

abnormal neuroanatomy | adult stage, with Scer\GAL4^elav-C155

(Dinh et al., 2021)

abnormal neuroanatomy | adult stage, with Scer\GAL4^nSyb.PU

(Chen et al., 2014)

abnormal neuroanatomy | adult stage, with Scer\GAL4^ple.PF

(Zhu et al., 2016)

abnormal neuroanatomy | adult stage | conditional, with Scer\GAL4^elav.PU

(Kontopoulos et al., 2006)

abnormal neuroanatomy | adult stage | progressive, with Scer\GAL4^NP6510

(Riemensperger et al., 2013)

abnormal neuroanatomy | progressive, with Scer\GAL4^ple.PF

(Botella et al., 2008)

abnormal oxidative stress response | adult stage, with Scer\GAL4^elav.PU

(Chen et al., 2014)

abnormal smell perception | adult stage, with Scer\GAL4^ple.PU

(Chen et al., 2014)

abnormal smell perception | adult stage | progressive, with Scer\GAL4^elav.PU

(Chen et al., 2014)

chemical sensitive, with Scer\GAL4^elav-C155

(Jahromi et al., 2015)

decreased cell number | adult stage, with Scer\GAL4^elav-C155

(Dinh et al., 2021, Kong et al., 2015)

decreased cell number | adult stage, with Scer\GAL4^nSyb.PU

(Chen et al., 2014)

decreased cell number | adult stage, with Scer\GAL4^ple.PF

(Cunningham et al., 2018)

decreased cell number | adult stage | progressive, with Scer\GAL4^Ddc.PU

(Yan et al., 2019)

decreased cell number | adult stage | progressive, with Scer\GAL4^GMR.long

(Yan et al., 2019)

decreased cell number | nutrition conditional, with Scer\GAL4^ple.PF

(Zhu et al., 2016)

decreased rate of flight behavior, with Scer\GAL4^da.PU

(Diaw et al., 2023)

decreased rate of movement | adult stage | progressive, with Scer\GAL4^nSyb.PU

(Chen et al., 2014)

short lived, with Scer\GAL4^da.PU

(Diaw et al., 2023)

short lived, with Scer\GAL4^Ddc.PU

(Yan et al., 2019)

short lived, with Scer\GAL4^elav-C155

(Jahromi et al., 2015, Kong et al., 2015)

short lived | nutrition conditional, with Scer\GAL4^ple.PF

(Zhu et al., 2016)

Phenotype Manifest In

adult dopaminergic PAM neuron | decreased number, with Scer\GAL4^elav-C155

(Dinh et al., 2021)

adult dopaminergic PAM neuron | progressive, with Scer\GAL4^NP6510

(Riemensperger et al., 2013)

dopamine neuron & adult brain, with Scer\GAL4^elav.PLu

(Feany and Bender, 2000)

dopaminergic neuron, with Scer\GAL4^Ddc.PL

(Yang et al., 2003, Auluck et al., 2002)

dopaminergic neuron, with Scer\GAL4^ple.PF

(Bayersdorfer et al., 2010)

dopaminergic neuron | adult stage, with Scer\GAL4^elav-C155

(Kong et al., 2015)

dopaminergic neuron | conditional, with Scer\GAL4^elav.PU

(Kontopoulos et al., 2006)

dopaminergic neuron | progressive, with Scer\GAL4^ple.PF

(Botella et al., 2008)

dopaminergic PPL1 neuron, with Scer\GAL4^ple.PF

(Cunningham et al., 2018)

dopaminergic PPM1 neuron | adult stage, with Scer\GAL4^ple.PF

(Zhu et al., 2016)

dopaminergic PPM2 neuron | adult stage, with Scer\GAL4^nSyb.PU

(Chen et al., 2014)

dopaminergic PPM2 neuron | adult stage, with Scer\GAL4^ple.PF

(Zhu et al., 2016)

dopaminergic PPM3 neuron | progressive, with Scer\GAL4^Ddc.PU

(Yan et al., 2019)

dorso-lateral dopaminergic neuron, with Scer\GAL4^Ddc.PL

(Auluck et al., 2002)

eye photoreceptor cell | progressive, with Scer\GAL4^GMR.long

(Yan et al., 2019)

ommatidium | progressive, with Scer\GAL4^GMR.long

(Yan et al., 2019)

retina, with Scer\GAL4^GMR.PF

(Feany and Bender, 2000)

retina | progressive, with Scer\GAL4^GMR.long

(Yan et al., 2019)

Detailed Description

Statement

Reference

Expressing Hsap\SNCA^A30P.UAS under the control of Scer\GAL4^elav-C155 leads to adults showing a progressive decrease in climbing ability; the adult brain (15 days old) shows a decrease in TH+ PAM neurons.

(Dinh et al., 2021)

The expression of Hsap\SNCA^A30P.UAS under the control of Scer\GAL4^GMR.long leads to progressive retinal generation: while 1-day old adults show normal retinal morphology, 30-days old adults show severe defects, namely apparent loss of photoreceptor neurons along with vacuole formation.

Adults expressing Hsap\SNCA^A30P.UAS under the control of Scer\GAL4^Ddc.PU show age-dependent impairment in climbing ability, associated with a progressive decrease in PPM3 neurons, despite of no significant changes in other DA neurons (PAL, PPM1/2, PPL1 and PPL2 clusters) as compared to controls.

(Yan et al., 2019)

The expression of Hsap\SNCA^A30P.UAS under the control of Scer\GAL4^elav.PU leads to a progressive decline in adult locomotion capacity (i.e. climbing assays), as compared to controls.

(Chen and Tully, 2018)

Expressing Hsap\SNCA^A30P.UAS under the control of Scer\GAL4^ple.PF induces a progressive decrease in adult climbing capacity and results in 21-days old adults raised at 29[o]C exhibiting significantly fewer PPL1 neurons than age-matched controls; there is no obvious effect on lifespan.

(Cunningham et al., 2018)

Individuals expressing Hsap\SNCA^A30P.UAS under the control of Scer\GAL4^elav-C155 present a progressive decrease in climbing ability, as compared to controls

(Issa et al., 2018)

Adult flies expressing Hsap\SNCA^{A30P.Scer\UAS} under the control of Scer\GAL4^ple.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.

(Zhu et al., 2016)

Expression of Hsap\SNCA^{A30P.Scer\UAS} under the control of Scer\GAL4^elav-C155 results in a significant reduction in lifespan as compared to controls. These flies exhibit a significantly lower sedation time in response to acute ethanol exposure, and also show a significant longer recovery time, as compared to controls.

(Jahromi et al., 2015)

Flies expressing Hsap\SNCA^{A30P.Scer\UAS} under the control of Scer\GAL4^elav-C155 show defects in climbing ability. This phenotype is partially suppressed when the flies are fed the natural antioxidant decalepis hamiltonii (Dh).

Locomotor rhythm and level of physical activity are disrupted in flies expressing Hsap\SNCA^{A30P.Scer\UAS} under the control of Scer\GAL4^elav-C155. This is partially suppressed when the flies are fed the natural antioxidant decalepis hamiltonii (Dh).

(Jahromi et al., 2015)

Expression of Hsap\SNCA^{A30P.Scer\UAS} under the control Scer\GAL4^elav-C155 leads to a decrease in lifespan, loss of dopaminergic cells, and progressive climbing defects, as compared to controls

(Kong et al., 2015)

Expression of Hsap\SNCA^{A30P.Scer\UAS} driven by Scer\GAL4^nSyb.PU leads to significant defects in climbing ability in 15 day old flies; climbing performance in mutants is significantly improved by administration of L-DOPA. 30 day old Scer\GAL4^nSyb.PU>Hsap\SNCA^{A30P.Scer\UAS} flies have significantly fewer dopamine neurons in the dorsomedial cluster, compared to controls.

Male Scer\GAL4^nSyb.PU>Hsap\SNCA^{A30P.Scer\UAS} flies that have been starved for 8 hours (to elevate baseline walking activity) show significant age-dependent (15 vs 30 day old) walking deficits (total distance walked, distance per episode, walking duration per episode, velocity, angular velocity and walking frequency) in an open field assay (no significant differences in controls). Young mutants do not show significant deficits compared to young controls, while aged mutants show significant defects in total distance walked, distance per episode, velocity and angular velocity compared to aged controls. Scer\GAL4^nSyb.PU>Hsap\SNCA^{A30P.Scer\UAS} aged males are significantly more centrophobic than young mutants, possibly showing elevated anxiety.

(Chen et al., 2014)

Ectopic expression of Hsap\SNCA^{A30P.Scer\UAS} under the control of Scer\GAL4^elav.PU results in an age-progressive deficit in climbing behavior as well as age-progressive impairment in odor acuity and odor discrimination (the olfaction defects are displayed even before the motor deficit is first manifested) in adult flies compared to wild-type controls. The odor discrimination deficit is not odor-specific.

The defective olfaction (odor acuity and odor discrimination impairment) seen in adult flies expressing Hsap\SNCA^{A30P.Scer\UAS} under the control of Scer\GAL4^elav.PU is (unlike in wild-type controls) further worsened under oxidative stress condition.

Impaired olfaction (deficit in both odor acuity and odor discrimination) is seen in adult flies expressing Hsap\SNCA^{A30P.Scer\UAS} under the control of the Scer\GAL4^ple.PU driver but not when expressed using the Scer\GAL4^ChAT.PU or the Scer\GAL4^Orco.PU driver.

(Chen et al., 2014)

Expression of Hsap\SNCA^{A30P.Scer\UAS} under the control of Scer\GAL4^ple.PF does not result in a loss of dopaminergic neurons in 55-day old flies.

(Navarro et al., 2014)

Flies expressing Hsap\SNCA^{A30P.Scer\UAS} under the control of either Scer\GAL4^elav-C155, Scer\GAL4^Ddc.PL or Scer\GAL4^NP6510 show an accelerated age-dependent decline in locomotor performance in a startle-induced negative geotaxis (SING) assay compared to controls.

Expression of Hsap\SNCA^{A30P.Scer\UAS} under the control of either Scer\GAL4^ple.PF or Scer\GAL4^Trh.PB has no significant effect on locomotor performance in a SING assay.

Flies expressing Hsap\SNCA^{A30P.Scer\UAS} under the control of Scer\GAL4^GMR58E02 show an accelerated age-dependent decline in locomotor performance in a SING assay compared to Scer\GAL4^GMR58E02 controls (which themselves show faster decline in the SING assay than wild type).

Expression of Hsap\SNCA^{A30P.Scer\UAS} under the control of Scer\GAL4^NP6510 results in an apparent decrease in Scer\GAL4^NP6510-positive dopaminergic terminals connected to the middle part of the mushroom body β lobes and the tip of the β' lobes in 3 day old flies compared to wild-type controls (analysed using the "split-GFP reconstitution across synaptic partners" (GRASP) technique). In 20 day old mutant flies there is an almost complete disappearance of dopaminergic connections, particularly in the β' lobes. There is no overt loss of dopaminergic neuron cell bodies in the protocerebral anterior medial cluster and projections of non-dopaminergic Scer\GAL4^NP6510-positive neurons towards the fan-shaped bodies are normal.

(Riemensperger et al., 2013)

Flies expressing Hsap\SNCA^{A30P.Scer\UAS} under the control of Scer\GAL4^elav-C155 exhibit a 59% licking activity and 50.7% attempted copulation activity, relative to wild-type. These flies exhibit 27.3% fewer copulations compared to wild-type. Hsap\SNCA^{A30P.Scer\UAS}-expressing males perform less sexual activity, relative to Oregon-R males.

Expression of Hsap\SNCA^{A30P.Scer\UAS} under the control of Scer\GAL4^elav-C155 does not affect climbing ability at 6 days of age. Measurement at 21 days reveals significant locomotor dysfunction, reflecting a 28% reduction in climbing ability.

(Shaltiel-Karyo et al., 2012)

Three-day-old flies overexpressing Hsap\SNCA^{A30P.Scer\UAS} under the control of Scer\GAL4^ple.PF show a 20% reduction in the number of dopaminergic neurons compared to control flies. In 35-day-old flies there is an additional decrease in the number of dopaminergic neurons by 28% compared to those observed in 3-day-old flies, while control flies show no significant neurodegeneration.

Overexpression of Hsap\SNCA^{A30P.Scer\UAS} under the control of Scer\GAL4^ple.PF leads to an age-dependent decline in motor abilities. However, climbing ability is not affected.

(Bayersdorfer et al., 2010)

Flies expressing Hsap\SNCA^{A30P.Scer\UAS} in dopaminergic neurons under the control of Scer\GAL4^ple.PF exhibit age-dependent neurodegeneration. No neuron loss is seen at days 15, but increased neurodegeneration compared to controls is seen by 25 days. No loss of dopaminergic neurons is seen in age-matched wild type flies.

Expression of Hsap\SNCA^{A30P.Scer\UAS} under the control of Scer\GAL4^ple.PF enhances the hypoxia-induced dopaminergic neuron degeneration seen in control flies.

(Botella et al., 2008)

20 day old flies expressing Hsap\SNCA^{A30P.Scer\UAS} under the control of Scer\GAL4^elav.PU show a loss of dorsomedial dopamine neurons in the brain.

(Kontopoulos et al., 2006)

20 day old flies expressing Hsap\SNCA^{A30P.Scer\UAS} under the control of Scer\GAL4^Ddc.PL have a 50% reduction in the number of dopaminergic neurons in the dorsomedial clusters of the brain.

(Yang et al., 2003)

20 day old flies expressing Hsap\SNCA^{A30P.Scer\UAS} under the control of Scer\GAL4^Ddc.PL show marked loss of neurons in the dorsomedial dopaminergic clusters. Neuron loss is more variable in the dorsolateral-1 dopaminergic clusters, ranging from no loss of neurons to as much as 50% of neurons being lost.

(Auluck et al., 2002)

Expression of Hsap\SNCA^{A30P.Scer\UAS} under the control of Scer\GAL4^Cha.7.4 does not affect cholinergic neurons in the optic lamina.

(Wittmann et al., 2001)

Overall brain volume, including the outer cellular cortex layer containing neuronal and glial cell bodies and central neuropil areas, and overall brain architecture are preserved in 60 day old flies expressing Hsap\SNCA^{A30P.Scer\UAS} under the control of Scer\GAL4^elav.PLu. These flies show a marked, age-dependent loss of dorsomedial dopaminergic neurons. All the major serotonergic cell groups are present in 30 day old flies. 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. The inclusions have a relatively homogeneous core and are edged by radiating filaments projecting into a surrounding halo. The filaments are 7-10nm in diameter and are sometimes associated with cellular organelles. Granular material is intermixed with loosely packed filaments in less compact inclusions. 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\SNCA^{A30P.Scer\UAS} under the control of Scer\GAL4^elav.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\SNCA^{A30P.Scer\UAS} under the control of Scer\GAL4^GMR.PF show retinal degeneration that is detectable by 10 days, and marked at 30 days after eclosion.

(Feany and Bender, 2000)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

Hsap\SNCA^A30P.UAS, Scer\GAL4^Ddc.PL has abnormal locomotor rhythm | adult stage phenotype, suppressible by anne^KK107621, Scer\GAL4^Ddc.PL

(Dhanushkodi et al., 2023)

Hsap\SNCA^A30P.UAS, Scer\GAL4^elav-C155 has abnormal locomotor behavior | adult stage | progressive phenotype, suppressible by TP53INP^FENLL.UAS, Scer\GAL4^elav-C155

(Dinh et al., 2021)

Hsap\SNCA^A30P.UAS, Scer\GAL4^elav-C155 has abnormal locomotor behavior | adult stage | progressive phenotype, suppressible by TP53INP^long.UAS, Scer\GAL4^elav-C155

(Dinh et al., 2021)

Hsap\SNCA^A30P.UAS, Scer\GAL4^elav-C155 has decreased cell number | adult stage phenotype, suppressible by TP53INP^long.UAS, Scer\GAL4^elav-C155

(Dinh et al., 2021)

Hsap\SNCA^A30P.UAS, Scer\GAL4^elav-C155 has abnormal neuroanatomy | adult stage phenotype, suppressible by TP53INP^long.UAS, Scer\GAL4^elav-C155

(Dinh et al., 2021)

Hsap\SNCA^A30P.UAS, Scer\GAL4^Ddc.PU has decreased cell number | adult stage | progressive phenotype, suppressible by Ire1^GD3071, Scer\GAL4^Ddc.PU

(Yan et al., 2019)

Hsap\SNCA^A30P.UAS, Scer\GAL4^Ddc.PU has short lived phenotype, suppressible by Ire1^HMS03003, Scer\GAL4^Ddc.PU

(Yan et al., 2019)

Hsap\SNCA^A30P.UAS, Scer\GAL4^Ddc.PU has short lived phenotype, suppressible by Atg7^GD11671, Scer\GAL4^Ddc.PU

(Yan et al., 2019)

Hsap\SNCA^A30P.UAS, Scer\GAL4^Ddc.PU has abnormal locomotor behavior | adult stage | progressive phenotype, suppressible by Ire1^HMS03003, Scer\GAL4^Ddc.PU

(Yan et al., 2019)

Hsap\SNCA^A30P.UAS, Scer\GAL4^Ddc.PU has decreased cell number | adult stage | progressive phenotype, suppressible by Ire1^HMS03003, Scer\GAL4^Ddc.PU

(Yan et al., 2019)

Hsap\SNCA^A30P.UAS, Scer\GAL4^Ddc.PU has decreased cell number | adult stage | progressive phenotype, suppressible by Atg7^GD11671, Scer\GAL4^Ddc.PU

(Yan et al., 2019)

Hsap\SNCA^A30P.UAS, Scer\GAL4^Ddc.PU has abnormal locomotor behavior | adult stage | progressive phenotype, suppressible by Atg7^GD11671, Scer\GAL4^Ddc.PU

(Yan et al., 2019)

Hsap\SNCA^A30P.UAS, Scer\GAL4^Ddc.PU has short lived phenotype, suppressible by Ire1^GD3071, Scer\GAL4^Ddc.PU

(Yan et al., 2019)

Hsap\SNCA^A30P.UAS, Scer\GAL4^Ddc.PU has abnormal locomotor behavior | adult stage | progressive phenotype, suppressible by Ire1^GD3071, Scer\GAL4^Ddc.PU

(Yan et al., 2019)

Hsap\SNCA^A30P.UAS, Scer\GAL4^ple.PF has decreased cell number | adult stage phenotype, suppressible by st^UAS.Venus, Scer\GAL4^ple.PF

(Cunningham et al., 2018)

Hsap\SNCA^A30P.UAS, Scer\GAL4^ple.PF has abnormal locomotor behavior | adult stage | progressive phenotype, suppressible by st^UAS.Venus, Scer\GAL4^ple.PF

(Cunningham et al., 2018)

Hsap\SNCA^A30P.UAS, Scer\GAL4^elav-C155 has abnormal locomotor behavior | adult stage | progressive phenotype, suppressible by Hsap\LAMP2^UAS.cIa, Scer\GAL4^elav-C155

(Issa et al., 2018)

Hsap\SNCA^A30P.UAS, Scer\GAL4^ple.PF has abnormal neuroanatomy phenotype, suppressible by ple^GD1181, Scer\GAL4^ple.PF

(Bayersdorfer et al., 2010)

Hsap\SNCA^A30P.UAS, Scer\GAL4^ple.PF has abnormal locomotor behavior phenotype, suppressible by ple^GD1181, Scer\GAL4^ple.PF

(Bayersdorfer et al., 2010)

Hsap\SNCA^A30P.UAS, Scer\GAL4^ple.PF has abnormal neuroanatomy | progressive phenotype, suppressible by Hsap\SOD1^UAS.cPa, Scer\GAL4^ple.PF

(Botella et al., 2008)

Hsap\SNCA^A30P.UAS, Scer\GAL4^elav.PU has abnormal neuroanatomy | adult stage | conditional phenotype, suppressible by Sin3A⁰⁸²⁶⁹

(Kontopoulos et al., 2006)

Hsap\SNCA^A30P.UAS, Scer\GAL4^Ddc.PL has abnormal neuroanatomy phenotype, suppressible by Hsap\PRKN^UAS.cYa, Scer\GAL4^Ddc.PL

(Yang et al., 2003)

Other

Statement

Reference

Hsap\SNCA^A30P.UAS, Scer\GAL4^Ddc.PL, anne^KK107621 has decreased cell number | adult stage phenotype

(Dhanushkodi et al., 2023)

Phenotype Manifest In

Suppressed by

Statement

Reference

Hsap\SNCA^A30P.UAS, Scer\GAL4^elav-C155 has adult dopaminergic PAM neuron | decreased number phenotype, suppressible by TP53INP^long.UAS, Scer\GAL4^elav-C155

(Dinh et al., 2021)

Hsap\SNCA^A30P.UAS, Scer\GAL4^GMR.long has ommatidium | progressive phenotype, suppressible | partially by Ire1^GD3071, Scer\GAL4^GMR.long

(Yan et al., 2019)

Hsap\SNCA^A30P.UAS, Scer\GAL4^GMR.long has ommatidium | progressive phenotype, suppressible | partially by Ire1^HMS03003, Scer\GAL4^GMR.long

(Yan et al., 2019)

Hsap\SNCA^A30P.UAS, Scer\GAL4^GMR.long has retina | progressive phenotype, suppressible | partially by Ire1^GD3071, Scer\GAL4^GMR.long

(Yan et al., 2019)

Hsap\SNCA^A30P.UAS, Scer\GAL4^GMR.long has retina | progressive phenotype, suppressible | partially by Ire1^HMS03003, Scer\GAL4^GMR.long

(Yan et al., 2019)

Hsap\SNCA^A30P.UAS, Scer\GAL4^Ddc.PU has dopaminergic PPM3 neuron | progressive phenotype, suppressible by Ire1^GD3071, Scer\GAL4^Ddc.PU

(Yan et al., 2019)

Hsap\SNCA^A30P.UAS, Scer\GAL4^Ddc.PU has dopaminergic PPM3 neuron | progressive phenotype, suppressible by Ire1^HMS03003, Scer\GAL4^Ddc.PU

(Yan et al., 2019)

Hsap\SNCA^A30P.UAS, Scer\GAL4^Ddc.PU has dopaminergic PPM3 neuron | progressive phenotype, suppressible by Atg7^GD11671, Scer\GAL4^Ddc.PU

(Yan et al., 2019)

Hsap\SNCA^A30P.UAS, Scer\GAL4^ple.PF has dopaminergic PPL1 neuron phenotype, suppressible by st^UAS.Venus, Scer\GAL4^ple.PF

(Cunningham et al., 2018)

Hsap\SNCA^A30P.UAS, Scer\GAL4^ple.PF has dopaminergic neuron phenotype, suppressible by ple^GD1181, Scer\GAL4^ple.PF

(Bayersdorfer et al., 2010)

Hsap\SNCA^A30P.UAS, Scer\GAL4^ple.PF has dopaminergic neuron | progressive phenotype, suppressible by Hsap\SOD1^UAS.cPa, Scer\GAL4^ple.PF

(Botella et al., 2008)

Hsap\SNCA^A30P.UAS, Scer\GAL4^elav.PU has dopaminergic neuron | conditional phenotype, suppressible by Sin3A⁰⁸²⁶⁹

(Kontopoulos et al., 2006)

Hsap\SNCA^A30P.UAS, Scer\GAL4^Ddc.PL has dopaminergic neuron phenotype, suppressible by Hsap\PRKN^UAS.cYa, Scer\GAL4^Ddc.PL

(Yang et al., 2003)

Other

Statement

Reference

Hsap\SNCA^A30P.UAS, Scer\GAL4^Ddc.PL, anne^KK107621 has adult dopaminergic neuron | decreased number phenotype

(Dhanushkodi et al., 2023)

Additional Comments

Genetic Interactions

Statement

Reference

Xenogenetic Interactions

Statement

Reference

The number of dopaminergic neurons in Hsap\SNCA^{A30P.Scer\UAS} flies also expressing ple^GD1181 does not change from 3 to 35 days indicating a strong suppression effect by the ple^GD1181 line (when both are expressed under the control of Scer\GAL4^ple.PF).

Co-expression of ple^GD1181 with Hsap\SNCA^{A30P.Scer\UAS} (both under the control of Scer\GAL4^ple.PF) rescues the age-dependent decline in motor abilities seen upon Hsap\SNCA^{A30P.Scer\UAS} overexpression.

(Bayersdorfer et al., 2010)

Expression of Hsap\SOD1^Scer\UAS.cPa suppresses the dopaminergic neuron degeneration seen when Hsap\SNCA^{A30P.Scer\UAS} is expressed under the control of Scer\GAL4^ple.PF. The reduction in climbing ability is also suppressed.

(Botella et al., 2008)

Sin3A⁰⁸²⁶⁹ rescues the progressive loss of dorsomedial dopamine neurons in the brain seen in flies expressing Hsap\SNCA^{A30P.Scer\UAS} under the control of Scer\GAL4^elav.PU.

(Kontopoulos et al., 2006)

The reduction in the number of dopaminergic neurons in the dorsomedial clusters of the brain seen in 20 day old flies expressing Hsap\SNCA^{A30P.Scer\UAS} under the control of Scer\GAL4^Ddc.PL is suppressed by coexpression of Hsap\PARK2^Scer\UAS.cYa.

(Yang et al., 2003)

Complementation and Rescue Data

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Images (0)

Mutant

Wild-type

Stocks (1)

Bloomington

8147

w^*; P{UAS-Hsap\SNCA.A30P}40.1

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (2)

Reported As

Symbol Synonym

Hsap\SNCA^{A30P.Scer\UAS}

Hsap\SNCA^A30P.UAS

Name Synonyms

Secondary FlyBase IDs

References (45)

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