A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Allele Dmel\Pink1B9

General Information
SymbolDmel\Pink1B9SpeciesD. melanogaster
NameFlyBase IDFBal0193144
Feature typealleleAssociated geneDmel\Pink1
Also Known AsdPink1B9
Allele classloss of function allele
MutagenP-element activity
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Description
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FB2013_03
FB2013_02
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hide Nature of the Allele
Allele class
Mutagen
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
Imprecise excision of the insertion, resulting in a deletion of 570bp of Pink1 sequences.
Cytology
hide Phenotypic Data
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hide Phenotype Manifest In
dopamine neuron & adult brain
mitochondrial inner membrane & indirect flight muscle
mitochondrial outer membrane & indirect flight muscle
mitochondrion & dopamine neuron & adult brain
mitochondrion & dopaminergic neuron
mitochondrion & dorso-lateral dopaminergic neuron
mitochondrion & indirect flight muscle
myofibril & indirect flight muscle
hide Detailed Description
Statement
Reference
10 day old mutant flies have impaired climbing ability compared to controls. Mutant flies have thoracic indentations.
Pink1[B9] flies are sensitive to heat shock stress and die sooner than control flies.
The mitochondria in the indirect flight muscles of mutant adults appear enlarged and clumped compared to controls.
The flight defects of mutant animals are significantly improved by feeding with vitamin K[[2]] (MK-4 and MK-8 forms tested). The mitochondrial morphology defects of mutant larvae are partially rescued by feeding with vitamin K[[2]] (MK-4 form tested).
Mutant adults often have abnormal thoraces with dents in the mid-anterior region. As the mutant adults age, they develop abnormal wing postures, with the percentage of affected flies increasing with age. The mutant adults also show a progressive loss of climbing ability and have a shorter lifespan than normal. Mitochondria in the indirect flight muscles of one day old mutant adults are abnormally fused with one another and the structures of the mitochondrial cristae are unclear. Mitochondria in the mutant dopaminergic neurons of the adult brain form spherical aggregates (in contrast to the long tubular network seen in wild type). 25 day old adults show loss of dopaminergic neurons in the protocerebral posterior lateral 1 (PPL1) and protocerebral posterior medial 1 and 2 (PPM1/2) clusters of the brain.
Mutant flies have a downturned wing position and crushed thorax and are flightless. Mutants have unusually large swollen mitochondria in the dopaminergic neurons.
5 day old adult mutant flies have an abnormal wing posture. Indirect flight muscles are thin, atrophic and disorganised in these animals. Some of the mitochondria in the indirect flight muscles appear grossly enlarged, with the inner membrane being disorganised or disintegrated. Prominent mitochondrial aggregates form in the dorsolateral protocerebral posterior DA (dopaminergic) neuron cluster in Pink1[B9] animals, and in addition tubular mitochondrial structure are also seen.
Mutant males have impaired sperm with swollen Nebenkern. 3 day old flies often show a downturned wing phenotype and they completely lack flight ability. Mutant adults show reduced climbing ability compared to controls both at 3 days and 30 days after eclosion. 85% of adults show a collapsed-thorax phenotype immediately after eclosion, particularly in the mid-anterior and anterolateral regions of the thorax. The percentage of flies showing this phenotype increases to 95% at 30 days after eclosion. The indirect flight muscles are reduced compared to wild-type and have an abnormal structure; the myofibrils are arranged irregularly and the mitochondria are immensely swollen with loss of the outer membrane. Apoptotic cells are detected in mutant indirect flight muscles but not in wild-type controls. The number of dopaminergic neurons in the dorsomedial and dorsolateral 1 (DL1) clusters of the brain is slightly but significantly reduced compared to controls in 30 day old adult flies. The number of dopaminergic neurons in the DL2 and posteriomedial clusters is not significantly altered in these animals. 3 day old Pink1B9 adults have a number of profoundly enlarged mitochondria in dopaminergic neurons in the dorsomedial, dorsolateral 1 and 2 and posteriomedial clusters of the brain. This enlarged mitochondrion phenotype progressively increases with age.
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Statement
Reference
Pink1B9 has flight defective phenotype, enhanceable by heix[+]/heix1
Pink1B9 has flight defective phenotype, enhanceable by heix[+]/heixNP5301
Pink1B9 has flight defective phenotype, enhanceable by heix2/heix[+]
Pink1B9 has flight defective phenotype, enhanceable by heixk11403/heix[+]
hideNOT Enhanced by
Statement
Reference
hideSuppressed by
Statement
Reference
Pink1B9 has short lived phenotype, suppressible by Pgam51
Pink1B9 has short lived phenotype, suppressible by Pgam5NP0568
Pink1B9 has visible phenotype, suppressible by opa1-like[+]/opa1-likeEY09863
Pink1B9 has visible phenotype, suppressible by Pgam51
Pink1B9 has visible phenotype, suppressible by Pgam5NP0568
hideNOT suppressed by
Statement
Reference
Pink1B9 has flightless phenotype, non-suppressible by Drp12/Drp1[+]
Pink1B9 has flightless phenotype, non-suppressible by opa1-like[+]/opa1-likeEY09863
Pink1B9 has locomotor behavior defective phenotype, non-suppressible by park25
Pink1B9 has male sterile phenotype, non-suppressible by Drp1+t9.4
Pink1B9 has male sterile phenotype, non-suppressible by opa1-likes3475
Pink1B9 has visible phenotype, non-suppressible by Drp12/Drp1[+]
hideEnhancer of
Statement
Reference
hideNOT Enhancer of
Statement
Reference
hideSuppressor of
Statement
Reference
hideNOT Suppressor of
Statement
Reference
Pink1B9 is a non-suppressor of locomotor behavior defective phenotype of park25
hide Phenotype Manifest In
hideEnhanced by
Statement
Reference
hideSuppressed by
Statement
Reference
Pink1B9 has adult thorax phenotype, suppressible by opa1-like[+]/opa1-likeEY09863
Pink1B9 has adult thorax phenotype, suppressible by Pgam51
Pink1B9 has adult thorax phenotype, suppressible by Pgam5NP0568
Pink1B9 has dopamine neuron & adult brain phenotype, suppressible | partially by parkScer\UAS.T:Hsap\MYC/Scer\GAL4hs.PB
Pink1B9 has indirect flight muscle phenotype, suppressible by opa1-like[+]/opa1-likeEY09863
Pink1B9 has mitochondrial inner membrane & indirect flight muscle phenotype, suppressible by Drp1T:Zzzz\FLAG,T:Zzzz\TC,T:Ivir\HA1
Pink1B9 has mitochondrial inner membrane & indirect flight muscle phenotype, suppressible by opa1-like[+]/opa1-likeEY09863
Pink1B9 has mitochondrion & dopamine neuron & adult brain phenotype, suppressible | partially by parkScer\UAS.T:Hsap\MYC/Scer\GAL4ple.PF
Pink1B9 has mitochondrion & dopaminergic neuron phenotype, suppressible by Drp1Scer\UAS.T:Ivir\HA1/Scer\GAL4ple.PF
Pink1B9 has mitochondrion & dopaminergic neuron phenotype, suppressible by opa1-like[+]/opa1-likeEY09863
Pink1B9 has mitochondrion & dopaminergic neuron phenotype, suppressible by parkScer\UAS.T:Hsap\MYC/Scer\GAL4ple.PF
Pink1B9 has mitochondrion & dorso-lateral dopaminergic neuron phenotype, suppressible by Drp1T:Zzzz\FLAG,T:Zzzz\TC,T:Ivir\HA1
Pink1B9 has mitochondrion & dorso-lateral dopaminergic neuron phenotype, suppressible by opa1-like[+]/opa1-likeEY09863
Pink1B9 has mitochondrion & dorso-lateral dopaminergic neuron phenotype, suppressible by parkScer\UAS.T:Ivir\HA1/Scer\GAL4ple.PF
Pink1B9 has mitochondrion & indirect flight muscle phenotype, suppressible by Drp1T:Zzzz\FLAG,T:Zzzz\TC,T:Ivir\HA1
Pink1B9 has mitochondrion & indirect flight muscle phenotype, suppressible by opa1-like[+]/opa1-likeEY09863
Pink1B9 has mitochondrion phenotype, suppressible | partially by Pgam51
Pink1B9 has mitochondrion phenotype, suppressible | partially by Pgam5NP0568
Pink1B9 has wing phenotype, suppressible by MarfGD11094/Scer\GAL4hs.PB
Pink1B9 has wing phenotype, suppressible by opa1-like[+]/opa1-likeEY09863
Pink1B9 has wing phenotype, suppressible by Pgam51
Pink1B9 has wing phenotype, suppressible by Pgam5NP0568
hideNOT suppressed by
Statement
Reference
Pink1B9 has adult thorax phenotype, non-suppressible by Drp12/Drp1[+]
Pink1B9 has mitochondrion & dopaminergic neuron phenotype, non-suppressible by Drp12/Drp1[+]
Pink1B9 has wing phenotype, non-suppressible by Drp12/Drp1[+]
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Statement
Reference
hideNOT Suppressor of
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Statement
Reference
Expression of Trap1[Scer\UAS.cCa] under the control of either Scer\GAL4[da.G32] or Scer\GAL4[elav.PU] partially suppresses the thoracic indentation phenotype which is seen in Pink1[B9] flies. Expression of Trap1[Scer\UAS.cCa] under the control of Scer\GAL4[da.G32] in Pink1[B9] flies improves their climbing ability, lifespan, resistance to paraquat and mitochondrial function. Expression of Trap1[Scer\UAS.cCa] under the control of Scer\GAL4[elav.PU] improves climbing ability and mitochondrial respiration in Pink1[B9] flies.
Pgam5[1] Pink1[B9] double mutant flies are more sensitive to heat shock stress than either single mutant alone.
The mitochondrial morphology defects of Pink1[B9] larvae are partially rescued by expression of heix[Scer\UAS.cVa] under the control of Scer\GAL4[da.G32].
The defects in the adult thorax, the progressive abnormal wing posture phenotype, the progressive loss of climbing ability and the shorter lifespan seen in Pink1[B9] flies are suppressed if they are also mutant for either Pgam5[NP0568] or Pgam5[1]. The progressive abnormal wing posture phenotype, the progressive loss of climbing ability and the reduction in lifespan seen in Pink1[B9] flies are enhanced by expression of Pgam5[Scer\UAS.cIa] under the control of Scer\GAL4[da.G32]. The mitochondrial hyperfusion and loss of cristae of the mitochondria of indirect flight muscles of one day old Pink1[B9] adults is partially suppressed by either Pgam5[NP0568] or Pgam5[1]. The loss of dopaminergic neurons in the protocerebral posterior lateral 1 (PPL1) and protocerebral posterior medial 1 and 2 (PPM1/2) clusters of the brain that is seen in 25 day old Pink1[B9] adults is suppressed if the flies are also mutant for Pgam5[NP0568] or Pgam5[1].
The downturned wing, crushed thorax and flightless phenotypes of Pink1[B9] mutant flies are suppressed by expression of Drp1[Scer\UAS.T:Ivir\HA1] under the control of Scer\GAL4[hs.PB]. The downturned wing and crushed thorax phenotypes of Pink1[B9] mutant flies are enhanced by expression of Drp1[K38A.Scer\UAS.T:Ivir\HA1] under the control of Scer\GAL4[hs.PB]. The downturned wing, crushed thorax and flightless phenotypes of Pink1[B9] mutant flies are not suppressed by Drp1[2]/+. The downturned wing, crushed thorax and flightless phenotypes of Pink1[B9] mutant flies are not suppressed by expression of opa1-like[Scer\UAS.T:Zzzz\FLAG] under the control of Scer\GAL4[hs.PB]. The downturned wing and crushed thorax phenotypes but not the flightless phenotype of Pink1[B9] mutant flies is significantly suppressed by opa1-like[EY09863]/+. Expression of Marf[GD11094] under the control of Scer\GAL4[hs.PB] strongly suppresses the downturned wing and crushed thorax phenotypes of Pink1[B9] mutant flies and the flightless phenotype is partially suppressed. The downturned wing, crushed thorax and flightless phenotypes of Pink1[B9] mutant flies are not suppressed by expression of Marf[Scer\UAS.T:Zzzz\FLAG] under the control of Scer\GAL4[hs.PB]. The swollen mitochondria phenotype seen in dopaminergic neurons of Pink1[B9] mutants is suppressed by expression of one of park[Scer\UAS.T:Hsap\MYC] or Drp1[Scer\UAS.T:Ivir\HA1] under the control of Scer\GAL4[ple.PF]. The swollen mitochondria phenotype seen in dopaminergic neurons of Pink1[B9] mutants is not suppressed by Drp1[2]/+ but is significantly rescued by opa1-like[EY09863]/+.
The climbing ability of park[25] Pink1[B9] double mutants is not significantly different from the climbing ability of either single mutant. The climbing ability of HtrA2[Δ1] Pink1[B9] double mutants is not significantly different from the climbing ability of the Pink1[B9] single mutant. The defects in climbing ability that are seen in Pink1[B9] mutants are suppressed by expression of HtrA2[Scer\UAS.P\T.cTa] under the control of Scer\GAL4[Act].
Expression of park[Scer\UAS.T:Zzzz\FLAG,T:Hsap\COX4I1] under the control of Scer\GAL4[hs.PB] suppresses the mitochondrial swelling phenotype in Pink1[B9], park[1] double mutants to a great extent. Expression of park[Scer\UAS.T:Hsap\MYC] under the control of Scer\GAL4[hs.PB] partially suppresses the mitochondrial swelling phenotype in Pink1[B9], park[1] double mutants. Expression of park[T187A.Scer\UAS.T:Hsap\MYC] under the control of Scer\GAL4[hs.PB] partially suppresses the mitochondrial swelling phenotype in Pink1[B9], park[1] double mutants.
Pink1[B9] does not suppress the eye pigmentation loss seen in flies expressing HtrA2[Scer\UAS.cPa] under the control of Scer\GAL4[GMR.PF]. Pink1[B9] partially suppresses the rough eye phenotype seen when rho-7[Scer\UAS.cWa] is expressed under the control of Scer\GAL4[GMR.PF]. The normal abundance of interommatidial bristles is restored.
The abnormal wing posture phenotype and the abnormal morphology of the indirect flight muscles and their mitochondria which is seen in Pink1[B9] flies is suppressed by Drp1[T:Zzzz\FLAG,T:Zzzz\TC,T:Ivir\HA1] or by opa1-like[EY09863]/+. The mitochondrial aggregation phenotype seen in the dorsolateral protocerebral posterior DA (dopaminergic) neuron cluster in Pink1[B9] animals is suppressed by Drp1[T:Zzzz\FLAG,T:Zzzz\TC,T:Ivir\HA1] or by opa1-like[EY09863]/+. The mitochondrial aggregation phenotype seen in the dorsolateral protocerebral posterior DA (dopaminergic) neuron cluster in Pink1[B9] animals is suppressed by expression of park[Scer\UAS.T:Ivir\HA1] under the control of Scer\GAL4[ple.PF].
Expression of BuffyScer\UAS.cQa under the control of Scer\GAL4hs.PB markedly suppresses the adult wing and thorax phenotypes seen in Pink1B9 flies. The indirect flight muscle defects are also suppressed in these animals, although the flight defect is not rescued. Expression of parkScer\UAS.T:Hsap\MYC under the control of Scer\GAL4hs.PB markedly suppresses the downturned wing and crushed thorax phenotypes seen in Pink1B9 flies. The indirect flight muscle defects and the loss of dopaminergic neurons in the adult brain are also suppressed in these animals. The rescued flies show increased climbing speed and have some flight ability. Expression of parkScer\UAS.T:Hsap\MYC under the control of Scer\GAL4ple.PF significantly suppresses the enlarged mitochondria phenotype seen in the dopaminergic neurons of Pink1B9 adult brains. The thoracic muscle defects seen in park1 Pink1B9 double mutant flies are not increased in severity compared to either single mutant.
hide Xenogenetic Interactions
Statement
Reference
Scer\NDI1[Scer\UAS.cVa] (in the absence of a Scer\GAL4 driver) rescues the sterility of Pink1[B9] male flies. Expression of Scer\NDI1[Scer\UAS.cVa] under the control of Scer\GAL4[da.G32] partially suppresses the flight defects of Pink1[B9] flies. The defects in organisation of the mitochondria which are seen in the indirect flight muscles of Pink1[B9] flies are also partially suppressed by expression of Scer\NDI1[Scer\UAS.cVa] under the control of Scer\GAL4[da.G32]. Expression of Zzzz\AOX[Scer\UAS.cFa] under the control of Scer\GAL4[da.G32] does not suppress the male sterility, flight defects or defects in mitochondrial morphology seen in Pink1[B9] flies.
hide Complementation & Rescue Data
Rescued by
Partially rescued by
Not rescued by
Comments
Expression of Pink1[K337R.D479A.D501A.Scer\UAS.T:Ivir\HA1] under the control of Scer\GAL4[hs.PB] fails to rescue the apparent behavioural phenotypes of Pink1[B9] mutants. Impaired mitochondria in the indirect flight muscle of Pink1[B9] mutants are not recovered by Pink1[K337R.D479A.D501A.Scer\UAS.T:Ivir\HA1] expression under the control of Scer\GAL4[hs.PB]. Expression of Pink1[Scer\UAS.T:Ivir\HA1] under the control of Scer\GAL4[hs.PB] almost fully rescues the apparent behavioural phenotypes of Pink1[B9] mutants. Similarly, impaired mitochondria in the indirect flight muscle of Pink1[B9] mutants are fully recovered by Pink1[Scer\UAS.T:Ivir\HA1] expression under the control of Scer\GAL4[hs.PB].
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Bloomington
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Discoverer
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Reported As
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Name Synonym
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hide References ( 15 )
Research paper
Costa et al., 2013, Cell Death Dis. 4: e467
Drosophila Trap1 protects against mitochondrial dysfunction in a PINK1/parkin model of Parkinson's disease. [FBrf0220561]
Ishida et al., 2012, PLoS ONE 7(2): e30265
Prevention of Apoptosis by Mitochondrial Phosphatase PGAM5 in the Mushroom Body Is Crucial for Heat Shock Resistance in Drosophila melanogaster. [FBrf0217492]
Kim et al., 2012, J. Biol. Chem. 287(9): 6628--6641
Glutathione s-transferase omega 1 activity is sufficient to suppress neurodegeneration in a Drosophila model of Parkinson disease. [FBrf0217543]
Vilain et al., 2012, PLoS Genet. 8(1): e1002456
The Yeast Complex I Equivalent NADH Dehydrogenase Rescues pink1 Mutants. [FBrf0217195]
Vos et al., 2012, Science 336(6086): 1306--1310
Vitamin K2 is a mitochondrial electron carrier that rescues pink1 deficiency. [FBrf0218543]
Imai et al., 2010, PLoS Genet. 6(12): e1001229
The Loss of PGAM5 Suppresses the Mitochondrial Degeneration Caused by Inactivation of PINK1 in Drosophila. [FBrf0212500]
Ziviani et al., 2010, Proc. Natl. Acad. Sci. U.S.A. 107(11): 5018--5023
Drosophila Parkin requires PINK1 for mitochondrial translocation and ubiquitinates Mitofusin. [FBrf0210308]
Park et al., 2009, Biochem. Biophys. Res. Commun. 378(3): 518--523
The PINK1-Parkin pathway is involved in the regulation of mitochondrial remodeling process. [FBrf0207317]
Tain et al., 2009, Cell Death Differ. 16(8): 1118--1125
Drosophila HtrA2 is dispensable for apoptosis but acts downstream of PINK1 independently from Parkin. [FBrf0208357]
Kim et al., 2008, Biochem. Biophys. Res. Commun. 377(3): 975--980
PINK1 controls mitochondrial localization of Parkin through direct phosphorylation. [FBrf0207333]
Whitworth et al., 2008, Dis. Model Mech. 1(2-3): 168--174
Rhomboid-7 and HtrA2/Omi act in a common pathway with the Parkinson's disease factors Pink1 and Parkin. [FBrf0206306]
Yang et al., 2008, Proc. Natl. Acad. Sci. U.S.A. 105(19): 7070--7075
Pink1 regulates mitochondrial dynamics through interaction with the fission/fusion machinery. [FBrf0205047]
Lee et al., 2007, Biochem. Biophys. Res. Commun. 358(2): 534--539
Loss of LRRK2/PARK8 induces degeneration of dopaminergic neurons in Drosophila. [FBrf0201118]
Park et al., 2006, Nature 441(7097): 1157--1161
Mitochondrial dysfunction in Drosophila PINK1 mutants is complemented by parkin. [FBrf0193630]
Erratum
Yang et al., 2008, Proc. Natl. Acad. Sci. U.S.A. 105(45): 17585
Correction for Yang et al., Pink1 regulates mitochondrial dynamics through interaction with the fission/fusion machinery. [FBrf0208866]