FlyBase Allele Report: Hsap\LRRK2[G2019S.UAS.Tag:MYC]

General Information

Symbol

Hsap\LRRK2^{G2019S.UAS.Tag:MYC}

Species

H. sapiens

Name

FlyBase ID

FBal0288352

Feature type

allele

Associated gene

Hsap\LRRK2

Associated Insertion(s)

Carried in Construct

P{UAS-LRRK2.G2019S.myc}

Also Known As

LRRK2 G2019S, LRRK2-G2019S, UAS-LRRK2-G2019S, UAS-LRRK2 G2019S

Key Links

Transgenic product class

missense_variant

(Ng et al., 2009)

Mutagen

in vitro construct

Nature of the Allele

Transgenic product class

missense_variant

(Ng et al., 2009)

Mutagen

in vitro construct

(Ng et al., 2009)

Progenitor genotype

Carried in construct

P{UAS-LRRK2.G2019S.myc}

Cytology

Description

UASt regulates expression of Hsap\LRRK2 containing a G2019S mutation, tagged with Tag:MYC at the C terminus.

(Ng et al., 2009)

Allele components

Component

Use(s)

Regulatory region(s)

UASt

binary expression system - regulatory region

Encoded product / tool

Hsap\LRRK2

Tagged with

Tag:MYC

epitope tag

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 Parkinson's disease 8

CEC

(Zhou et al., 2022, Basil et al., 2017)

CEA

(Hernandez-Diaz et al., 2022, Petridi et al., 2020, Sim et al., 2020, Nucifora et al., 2016)

model of Parkinson's disease

CEA

(Ng et al., 2017, Angeles et al., 2016, Ng et al., 2012, Ng et al., 2009)

CEC

(Angeles et al., 2014)

Modifiers Based on Experimental Evidence ( 1 )

Disease

Interaction

References

model of Parkinson's disease 8

is ameliorated by Hsap\PINK1^UAS.cUa

(Zhou et al., 2022)

is ameliorated by Hsap\AFDN^UAS.cBa

(Basil et al., 2017)

is exacerbated by cno^VDRC.cUa

(Basil et al., 2017)

is exacerbated by cno^RNAi.UAS.cUa

(Basil et al., 2017)

is ameliorated by Hsap\WSB1^UAS.cNa

(Nucifora et al., 2016)

is exacerbated by can^GD4085

(Nucifora et al., 2016)

is ameliorated by EndoB⁴

(Hernandez-Diaz et al., 2022)

is exacerbated by Pp2A-29B^GD17607

(Sim et al., 2020)

is exacerbated by mts^JF02805

(Sim et al., 2020)

is ameliorated by mts^UAS.cUa

(Sim et al., 2020)

is exacerbated by wdb^KK109072

(Sim et al., 2020)

is ameliorated by wrd^UAS.Tag:FLAG

(Sim et al., 2020)

is exacerbated by Rab10^UASp.YFP

(Petridi et al., 2020)

model of Parkinson's disease

is ameliorated by Hsap\PRKN^WT.UAS

(Ng et al., 2012, Ng et al., 2009)

is ameliorated by AMPKα^TD.UAS

(Ng et al., 2017, Ng et al., 2012)

is exacerbated by AMPKα^K57A.UAS

(Ng et al., 2012)

is exacerbated by AMPKα^GD736

(Ng et al., 2012)

is ameliorated by srl^UAS.cTa

(Ng et al., 2017)

is ameliorated by Hsap\PRDX3^UAS.cAa

(Angeles et al., 2014)

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

FlyBase curator comment: 'Parkinson's disease' subtype 'Parkinson's disease 8' is associated with mutations in the gene LRRK2, including the 'G2019S' mutation.

(Basil et al., 2017)

Disease-implicated variant(s)

This allele represents a human variant implicated in disease.

(Ng et al., 2009)

LRRK2:p.Gly2019Ser

(FlyBase curators, 2019-)

Variants Synonym(s)

Associated human disease model(s)

Parkinson disease 8

External database links

ClinVar: LRRK2_1940

Comments concerning this variant

Phenotypic Data

Phenotypic Class

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

(Ng et al., 2017, Ng et al., 2012)

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

(Angeles et al., 2014)

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

(Angeles et al., 2016)

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

(Ng et al., 2009)

abnormal locomotor behavior | adult stage | progressive, with Scer\GAL4^how-24B

(Ng et al., 2012)

abnormal neuroanatomy | adult stage, with Scer\GAL4^unspecified

(Angeles et al., 2016)

abnormal neuroanatomy | adult stage | progressive, with Scer\GAL4^Ddc.PL

(Ng et al., 2009)

abnormal neuroanatomy | progressive, with Scer\GAL4^Ddc.PU

(Angeles et al., 2014)

chemical sensitive | adult stage, with Scer\GAL4^Ddc.PL

(Ng et al., 2009)

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

(Ng et al., 2017)

decreased cell number | adult stage, with Scer\GAL4^unspecified

(Angeles et al., 2016)

short lived, with Scer\GAL4^Ddc.PL

(Ng et al., 2009)

short lived, with Scer\GAL4^elav.PU

(Angeles et al., 2014)

short lived | adult stage, with Scer\GAL4^unspecified

(Angeles et al., 2016)

Phenotype Manifest In

autolysosome | increased number | larval stage | nutrition conditional, with Scer\GAL4^Toll-6-D42

(Hernandez-Diaz et al., 2022)

autophagosome | increased number | larval stage | nutrition conditional, with Scer\GAL4^Toll-6-D42

(Hernandez-Diaz et al., 2022)

dopaminergic neuron, with Scer\GAL4^Ddc.PL

(Ng et al., 2012)

dopaminergic PPL1 neuron

(Angeles et al., 2016)

dopaminergic PPL1 neuron, with Scer\GAL4^Ddc.PL

(Ng et al., 2012)

dopaminergic PPL1 neuron | adult stage, with Scer\GAL4^Ddc.PL

(Ng et al., 2017)

dopaminergic PPL1 neuron | progressive, with Scer\GAL4^Ddc.PU

(Angeles et al., 2014)

dopaminergic PPM1 neuron | adult stage, with Scer\GAL4^unspecified

(Angeles et al., 2016)

dopaminergic PPM1 neuron | adult stage | progressive, with Scer\GAL4^Ddc.PL

(Ng et al., 2009)

dopaminergic PPM1 neuron | progressive, with Scer\GAL4^Ddc.PU

(Angeles et al., 2014)

dopaminergic PPM2 neuron | adult stage, with Scer\GAL4^unspecified

(Angeles et al., 2016)

dopaminergic PPM2 neuron | adult stage | chemical conditional, with Scer\GAL4^Ddc.PL

(Ng et al., 2009)

dopaminergic PPM3 neuron | adult stage, with Scer\GAL4^unspecified

(Angeles et al., 2016)

dopaminergic PPM3 neuron | adult stage | chemical conditional, with Scer\GAL4^Ddc.PL

(Ng et al., 2009)

dopaminergic PPM3 neuron | adult stage | progressive, with Scer\GAL4^Ddc.PL

(Ng et al., 2009)

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

(Angeles et al., 2014)

embryonic/larval neuromuscular junction | larval stage | nutrition conditional, with Scer\GAL4^Toll-6-D42

(Hernandez-Diaz et al., 2022)

flight muscle cell | progressive, with Scer\GAL4^how-24B

(Ng et al., 2012)

mitochondrion, with Scer\GAL4^Ddc.PL

(Ng et al., 2012)

mitochondrion, with Scer\GAL4^how-24B

(Angeles et al., 2014, Ng et al., 2012)

mitochondrion | adult stage, with Scer\GAL4^Ddc.PL

(Ng et al., 2017)

myofibril, with Scer\GAL4^how-24B

(Angeles et al., 2014)

NMJ bouton | larval stage | nutrition conditional, with Scer\GAL4^Toll-6-D42

(Hernandez-Diaz et al., 2022)

Detailed Description

Statement

Reference

Larvae expressing Hsap\LRRK2^{G2019S.UAS.Tag:MYC} under the control of Scer\GAL4^Toll-6-D42 show increased autophagosomes (Atg8-mCherry) and autolysosomes (Lamp-GFP) at NMJ boutons, under both fed and starved conditions.

(Hernandez-Diaz et al., 2022)

Expression of Hsap\LRRK2^{G2019S.Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^Ddc.PL leads to a loss of climbing ability, a loss of dopaminergic neurons in the PPL1 cluster, and a significant increase in mitochondrial size in dopaminergic neurons, as compared to controls.

(Ng et al., 2017)

Expression of Hsap\LRRK2^{G2019S.Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^unspecified neuronal driver results in a loss of dopaminergic neurons in the PPM1/2, PPm3 and PPL1 clusters as well as impaired locomotion and decreased lifespan in adult flies.

(Angeles et al., 2016)

Flies expressing Hsap\LRRK2^{G2019S.Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^Ddc.PU show age-dependent loss of dopamine neurons. Neuronal number is unaffected at 20 days, but there is a decrease in clusters PPM1/1, PPM3 and PPL1 at 60 days compared with controls. There is a marked decrease in climbing abilities compared to controls at 60 days. This reduction in climbing ability is suppressed when the flies are sustained on an Ebselen (Prx-mimic)-supplemented medium, and the dopaminergic neuron number is also suppressed. Treatment with the thiol-containing reducing anti-oxidant thiourea does not affect the phenotype.

The myofibrils of thoracic flight muscles expressing Hsap\LRRK2^{G2019S.Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^how-24B are loosely disorganised with irregular banding patterns. Feeding the flies with the Prx-mimic Ebselen restores the tightly organised structure seen in controls. The muscle mitochondria are swollen and less dense with vacuolation and fragmented cristae than controls, and this is also rescued by Ebelson. The levels of cytochrome c and ATP are lower than in controls, and these are also rescued by Ebelsen.

(Angeles et al., 2014)

Expression of Hsap\LRRK2^{G2019S.Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^how-24B produces prominent mitochondrial abnormalities in the flight muscles that become more severe with age. These flies also exhibit significant age-related climbing impairment relative to controls. The flight muscle phenotypes are rescued upon treatment with EGCG.

Expression of Hsap\LRRK2^{G2019S.Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^Ddc.PL results in the appearance of significantly enlarged mitochondria in dopaminergic neurons and loss of neurons in the protocerebral posterior lateral 1 (PPL1) cluster. These flies also exhibit climbing defects. All of these phenotypes are rescued upon treatment with EGCG. The climbing defects and loss of PPL1 dopaminergic neurons are also rescued upon treatment with AICAR, a direct pharmacological activator of AMPK. Flies treated with a commonly used AMPK inhibitor, Compound C, exhibit increased mortality.

(Ng et al., 2012)

Scer\GAL4^elav.PU-mediated expression of Hsap\LRRK2^{G2019S.Scer\UAS.T:Hsap\MYC} does not appear to compromise the overall anatomical integrity of the fly s brain up to 60 d after eclosion. Scanning electron microscope analysis reveals no apparent eye abnormalities in Scer\GAL4^GMR.PU Hsap\LRRK2^{G2019S.Scer\UAS.T:Hsap\MYC} flies at 20 d after eclosion. Similar observations are made when these flies are aged to 60 d. In 60 day old, but not 1 or 20 day old, flies expressing Hsap\LRRK2^{G2019S.Scer\UAS.T:Hsap\MYC} via Scer\GAL4^Ddc.PL, there is significant degeneration of DA neurons in the PPM clusters 1 and 3 (but not PAL, PPM2, PPL1 or PPL2) compared with age-matched normal control flies. 60 day old, but not 20 day old, flies expressing Hsap\LRRK2^{G2019S.Scer\UAS.T:Hsap\MYC} via Scer\GAL4^Ddc.PL record dramatically poorer climbing scores compared to controls. Flies expressing Hsap\LRRK2^{G2019S.Scer\UAS.T:Hsap\MYC} via Scer\GAL4^Ddc.PL have a reduced lifespan. There is an accelerated loss of DA neurons in the PPM 2/3 clusters of rotenone-treated flies expressing Hsap\LRRK2^{G2019S.Scer\UAS.T:Hsap\MYC} via Scer\GAL4^Ddc.PL, compared to controls.

(Ng et al., 2009)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

Hsap\LRRK2^{G2019S.UAS.Tag:MYC}, Scer\GAL4^Ddc.PL has abnormal locomotor behavior | adult stage phenotype, enhanceable by AMPKα^GD736, Scer\GAL4^Ddc.PL

(Ng et al., 2012)

Suppressed by

Statement

Reference

Hsap\LRRK2^{G2019S.UAS.Tag:MYC}, Scer\GAL4^Ddc.PL has abnormal locomotor behavior | adult stage phenotype, suppressible by AMPKα^TD.UAS, Scer\GAL4^Ddc.PL

(Ng et al., 2017)

Hsap\LRRK2^{G2019S.UAS.Tag:MYC}, Scer\GAL4^Ddc.PL has decreased cell number | adult stage phenotype, suppressible by AMPKα^TD.UAS, Scer\GAL4^Ddc.PL

(Ng et al., 2017)

Hsap\LRRK2^{G2019S.UAS.Tag:MYC}, Scer\GAL4^Ddc.PL has abnormal locomotor behavior | adult stage phenotype, suppressible | partially by srl^UAS.cTa, Scer\GAL4^Ddc.PL

(Ng et al., 2017)

Hsap\LRRK2^{G2019S.UAS.Tag:MYC}, Scer\GAL4^Ddc.PL has decreased cell number | adult stage phenotype, suppressible by srl^UAS.cTa, Scer\GAL4^Ddc.PL

(Ng et al., 2017)

Hsap\LRRK2^{G2019S.UAS.Tag:MYC}, Scer\GAL4^elav.PU has short lived phenotype, suppressible | partially by Hsap\PRDX3^UAS.cAa, Scer\GAL4^elav.PU

(Angeles et al., 2014)

Hsap\LRRK2^{G2019S.UAS.Tag:MYC}, Scer\GAL4^Ddc.PU has abnormal neuroanatomy | progressive phenotype, suppressible by Hsap\PRDX3^UAS.cAa, Scer\GAL4^Ddc.PU

(Angeles et al., 2014)

Hsap\LRRK2^{G2019S.UAS.Tag:MYC}, Scer\GAL4^Ddc.PU has abnormal locomotor behavior | adult stage phenotype, suppressible by Hsap\PRDX3^UAS.cAa, Scer\GAL4^Ddc.PU

(Angeles et al., 2014)

Hsap\LRRK2^{G2019S.UAS.Tag:MYC}, Scer\GAL4^how-24B has abnormal locomotor behavior | adult stage | progressive phenotype, suppressible by Hsap\PRKN^WT.UAS, Scer\GAL4^how-24B

(Ng et al., 2012)

NOT suppressed by

Statement

Reference

Hsap\LRRK2^{G2019S.UAS.Tag:MYC}, Scer\GAL4^Ddc.PL has abnormal locomotor behavior | adult stage phenotype, non-suppressible by AMPKα^TD.UAS/srl^KK100201, Scer\GAL4^Ddc.PL

(Ng et al., 2017)

Hsap\LRRK2^{G2019S.UAS.Tag:MYC}, Scer\GAL4^Ddc.PL has decreased cell number | adult stage phenotype, non-suppressible by AMPKα^TD.UAS/srl^KK100201, Scer\GAL4^Ddc.PL

(Ng et al., 2017)

Suppressor of

Statement

Reference

Hsap\LRRK2^{G2019S.UAS.Tag:MYC}, Scer\GAL4^elav.PU is a suppressor | partially of short lived phenotype of Hsap\PRDX3^UAS.cAa, Scer\GAL4^elav.PU

(Angeles et al., 2014)

Phenotype Manifest In

NOT Enhanced by

Statement

Reference

Hsap\LRRK2^{G2019S.UAS.Tag:MYC}, Scer\GAL4^Ddc.PL has dopaminergic PPL1 neuron phenotype, non-enhanceable by AMPKα^GD736, Scer\GAL4^Ddc.PL

(Ng et al., 2012)

Suppressed by

Statement

Reference

Hsap\LRRK2^{G2019S.UAS.Tag:MYC}, Scer\GAL4^Ddc.PL has dopaminergic PPL1 neuron | adult stage phenotype, suppressible by AMPKα^TD.UAS, Scer\GAL4^Ddc.PL

(Ng et al., 2017)

Hsap\LRRK2^{G2019S.UAS.Tag:MYC}, Scer\GAL4^Ddc.PL has mitochondrion | adult stage phenotype, suppressible by srl^UAS.cTa, Scer\GAL4^Ddc.PL

(Ng et al., 2017)

Hsap\LRRK2^{G2019S.UAS.Tag:MYC}, Scer\GAL4^Ddc.PL has dopaminergic PPL1 neuron | adult stage phenotype, suppressible by srl^UAS.cTa, Scer\GAL4^Ddc.PL

(Ng et al., 2017)

Hsap\LRRK2^{G2019S.UAS.Tag:MYC}, Scer\GAL4^Ddc.PU has dopaminergic PPM1 neuron | progressive phenotype, suppressible by Hsap\PRDX3^UAS.cAa, Scer\GAL4^Ddc.PU

(Angeles et al., 2014)

Hsap\LRRK2^{G2019S.UAS.Tag:MYC}, Scer\GAL4^Ddc.PU has dopaminergic PPM3 neuron | progressive phenotype, suppressible by Hsap\PRDX3^UAS.cAa, Scer\GAL4^Ddc.PU

(Angeles et al., 2014)

Hsap\LRRK2^{G2019S.UAS.Tag:MYC}, Scer\GAL4^Ddc.PU has dopaminergic PPL1 neuron | progressive phenotype, suppressible by Hsap\PRDX3^UAS.cAa, Scer\GAL4^Ddc.PU

(Angeles et al., 2014)

Hsap\LRRK2^{G2019S.UAS.Tag:MYC}, Scer\GAL4^how-24B has myofibril phenotype, suppressible by Hsap\PRDX3^UAS.cAa, Scer\GAL4^how-24B

(Angeles et al., 2014)

Hsap\LRRK2^{G2019S.UAS.Tag:MYC}, Scer\GAL4^how-24B has mitochondrion phenotype, suppressible by Hsap\PRDX3^UAS.cAa, Scer\GAL4^how-24B

(Angeles et al., 2014)

Hsap\LRRK2^{G2019S.UAS.Tag:MYC}, Scer\GAL4^Ddc.PL has dopaminergic neuron phenotype, suppressible by Hsap\PRKN^WT.UAS, Scer\GAL4^Ddc.PL

(Ng et al., 2012)

Hsap\LRRK2^{G2019S.UAS.Tag:MYC}, Scer\GAL4^Ddc.PL has mitochondrion phenotype, suppressible by Hsap\PRKN^WT.UAS, Scer\GAL4^Ddc.PL

(Ng et al., 2012)

Hsap\LRRK2^{G2019S.UAS.Tag:MYC}, Scer\GAL4^how-24B has flight muscle cell | progressive phenotype, suppressible by Hsap\PRKN^WT.UAS, Scer\GAL4^how-24B

(Ng et al., 2012)

Hsap\LRRK2^{G2019S.UAS.Tag:MYC}, Scer\GAL4^how-24B has mitochondrion phenotype, suppressible by Hsap\PRKN^WT.UAS, Scer\GAL4^how-24B

(Ng et al., 2012)

Hsap\LRRK2^{G2019S.UAS.Tag:MYC}, Scer\GAL4^Ddc.PL has dopaminergic PPM2 neuron | adult stage | chemical conditional phenotype, suppressible by Hsap\PRKN^WT.UAS, Scer\GAL4^Ddc.PL

(Ng et al., 2009)

Hsap\LRRK2^{G2019S.UAS.Tag:MYC}, Scer\GAL4^Ddc.PL has dopaminergic PPM3 neuron | adult stage | chemical conditional phenotype, suppressible by Hsap\PRKN^WT.UAS, Scer\GAL4^Ddc.PL

(Ng et al., 2009)

Hsap\LRRK2^{G2019S.UAS.Tag:MYC}, Scer\GAL4^Ddc.PL has dopaminergic PPM1 neuron | adult stage | progressive phenotype, suppressible by Hsap\PRKN^WT.UAS, Scer\GAL4^Ddc.PL

(Ng et al., 2009)

Hsap\LRRK2^{G2019S.UAS.Tag:MYC}, Scer\GAL4^Ddc.PL has dopaminergic PPM3 neuron | adult stage | progressive phenotype, suppressible by Hsap\PRKN^WT.UAS, Scer\GAL4^Ddc.PL

(Ng et al., 2009)

NOT suppressed by

Statement

Reference

Hsap\LRRK2^{G2019S.UAS.Tag:MYC}, Scer\GAL4^Ddc.PL has dopaminergic PPL1 neuron | adult stage phenotype, non-suppressible by AMPKα^TD.UAS/srl^KK100201, Scer\GAL4^Ddc.PL

(Ng et al., 2017)

NOT Suppressor of

Statement

Reference

Hsap\LRRK2^{G2019S.UAS.Tag:MYC}/Scer\GAL4^Toll-6-D42 is a non-suppressor of embryonic/larval neuromuscular junction | larval stage | nutrition conditional phenotype of EndoB⁴

(Hernandez-Diaz et al., 2022)

Hsap\LRRK2^{G2019S.UAS.Tag:MYC}/Scer\GAL4^Toll-6-D42 is a non-suppressor of NMJ bouton | larval stage | nutrition conditional phenotype of EndoB⁴

(Hernandez-Diaz et al., 2022)

Hsap\LRRK2^{G2019S.UAS.Tag:MYC}/Scer\GAL4^Toll-6-D42 is a non-suppressor of autophagosome | larval stage | decreased number | nutrition conditional phenotype of EndoB⁴

(Hernandez-Diaz et al., 2022)

Additional Comments

Genetic Interactions

Statement

Reference

Xenogenetic Interactions

Statement

Reference

Co-expression of AMPKα^TD.Scer\UAS fully suppresses the climbing defects and loss of dopaminergic neurons seen in flies expressing Hsap\LRRK2^{G2019S.Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^Ddc.PL.

Co-expression of srl^Scer\UAS.cTa partially suppresses the climbing defects and fully suppresses the loss of dopaminergic neurons and the mitochondrial size increase seen in flies expressing Hsap\LRRK2^{G2019S.Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^Ddc.PL.

Co-expression of both srl^KK100201 and AMPKα^TD.Scer\UAS fails to rescue the climbing defects and loss of dopaminergic neurons seen in flies expressing Hsap\LRRK2^{G2019S.Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^Ddc.PL.

(Ng et al., 2017)

Expression of Hsap\PRDX3^Scer\UAS.cAa suppresses the age-dependent PPM1, PPM3 and PPL1 dopaminergic neuron loss seen when Hsap\LRRK2^{G2019S.Scer\UAS.T:Hsap\MYC} is expressed under the control of Scer\GAL4^Ddc.PU. The reduction in climbing ability is also suppressed.

Expression of Hsap\PRDX3^Scer\UAS.cAa suppresses the defects in myofibril structure seen in the thoracic flight muscles of flies expressing Hsap\LRRK2^{G2019S.Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^how-24B. The increased frequency of deformed mitochondria and reduced levels of cytochrome c and ATP are also rescued by Hsap\PRDX3^Scer\UAS.cAa.

(Angeles et al., 2014)

Expression of Hsap\PARK2^WT.Scer\UAS suppresses the mitochondrial defects seen in dopaminergic neurons when Hsap\LRRK2^{G2019S.Scer\UAS.T:Hsap\MYC} is expressed under the control of Scer\GAL4^Ddc.PL.

Expression of SNF1A^GD736 enhances the climbing defects seen in flies expressing Hsap\LRRK2^{G2019S.Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^Ddc.PL. No further loss of the protocerebral posterior lateral 1 (PPL1) dopaminergic neurons is seen. The beneficial effects of EGCG treatment are completely abolished.

Expression of Hsap\PARK2^WT.Scer\UAS suppresses the mitochondrial defects seen in the flight muscles when Hsap\LRRK2^{G2019S.Scer\UAS.T:Hsap\MYC} is expressed under the control of Scer\GAL4^how-24B. The climbing defects are also rescued.

Expression of SNF1A^{K57A.Scer\UAS} enhances the climbing defects seen in flies expressing Hsap\LRRK2^{G2019S.Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^Ddc.PL. The beneficial effects of EGCG treatment on climbing ability are completely abolished. The beneficial effects of AICAR on climbing ability and protocerebral posterior lateral 1 (PPL1) dopaminergic neuron loss are also abolished.

Expression of SNF1A^TD.Scer\UAS suppresses the climbing defects seen in flies expressing Hsap\LRRK2^{G2019S.Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^Ddc.PL. The protocerebral posterior lateral 1 (PPL1) dopaminergic neuron loss is also suppressed. The low dopamine levels seen in flies expressing Hsap\LRRK2^{G2019S.Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^Ddc.PL are also restored in the presence of SNF1A^TD.Scer\UAS. Expression of SNF1A^TD.Scer\UAS also rescues the climbing defects and mitochondrial abnormalities seen when Hsap\LRRK2^{G2019S.Scer\UAS.T:Hsap\MYC} is expressed under the control of Scer\GAL4^how-24B.

(Ng et al., 2012)

The accelerated loss of DA neurons in the PPM 2/3 clusters of rotenone-treated flies expressing Hsap\LRRK2^{G2019S.Scer\UAS.T:Hsap\MYC} via Scer\GAL4^Ddc.PL is mitigated through co-expression of Hsap\PARK2^WT.Scer\UAS.

The significant degeneration of DA neurons in the PPM clusters 1 and 3 in 60 day old flies expressing Hsap\LRRK2^{G2019S.Scer\UAS.T:Hsap\MYC} via Scer\GAL4^Ddc.PL is mitigated through co-expression of Hsap\PARK2^WT.Scer\UAS.

(Ng et al., 2009)

Complementation and Rescue Data

Comments

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (2)

Reported As

Symbol Synonym

Hsap\LRRK2^{G2019S.Scer\UAS.T:Hsap\MYC}

Hsap\LRRK2^{G2019S.UAS.Tag:MYC}

Name Synonyms

Secondary FlyBase IDs

References (14)

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