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General Information
Symbol
Dmel\Pink1B9
Species
D. melanogaster
Name
FlyBase ID
FBal0193144
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
dPink1B9, PINKB9, PINK1[B9]
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference
Imprecise excision of the insertion, resulting in a deletion of 570bp of Pink1 sequences.
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
is ameliorated by mask10.22
is ameliorated by maskEY13048
is ameliorated by maskHMS01045
is ameliorated by maskKK100529
is exacerbated by ShmtGD8851
is ameliorated by Lrrke03680
is ameliorated by ParpCH1
is ameliorated by STUB1UAS.cCa
is ameliorated by Opa1s3475
is ameliorated by Opa1f02779
is ameliorated by mAcon11
is ameliorated by GstO2A.UAS
is ameliorated by Ucp4AUAS.cWa
is ameliorated by dj-1βC45A.UAS
is ameliorated by dj-1βUAS.cMa
is ameliorated by DJ-1αUAS.cUa
is ameliorated by Pink1UAS.cUa
is exacerbated by MiroUAS.cGa
is ameliorated by MiroJF02775
is ameliorated by miltJF03022
is ameliorated by MiroKK102189
is ameliorated by KhcJF01939
is ameliorated by Sirt1UAS.cGa
is ameliorated by Sirt1EP2300
is ameliorated by foxoUAS.cKd
is ameliorated by Sod2UAS.cUa
is ameliorated by cluUASp.cSa
is ameliorated by Trap1D6
is ameliorated by Trap1EY21851
is ameliorated by PEKGD5584
is ameliorated by ND-42SA.UAS
is exacerbated by heixNP5301
is exacerbated by heix1
is exacerbated by heix2
is exacerbated by heixk11403
is ameliorated by Pgam5NP0568
is ameliorated by Pgam51
is ameliorated by Trap1UAS.cCa
is exacerbated by rictorJF01370
is ameliorated by trcS292E.UAS.L
is ameliorated by rictorUAS.cHa
is ameliorated by trcL.UAS
is NOT ameliorated by RetMEN2B.UAS
is ameliorated by RetMEN2B.UAS
is ameliorated by RetMEN2B.UAS
is NOT ameliorated by RetMEN2B.UAS
is ameliorated by TER94UAS.cRa
is ameliorated by dnkUAS.cLa
Comments on Models/Modifiers Based on Experimental Evidence ( 4 )
 
No Parkinson's disease-related phenotypes are observed in Vps35MH20 Pink1B9 double heterozygotes.
No Parkinson's disease-related phenotypes are observed in Vps35E42 Pink1B9 double heterozygotes.
Drp1+t9.4 ameliorates the bioenergetic defects seen in the Pink1B9 Parkinson's model.
Analysis of Drosophila (Pink1B9) and mouse Parkinson disease models suggests that Complex I deficiency underlies, at least partially, the pathogenesis of recessive Parkinson disease.
Phenotypic Data
Phenotypic Class
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
Detailed Description
Statement
Reference
Pink1B9 hemizygotes show a fully penetrant thorax indentation phenotype and highly penetrant wing posture defect (dropped/held-up wings), as compared to controls.
Pink1B9 hemizygous male third instar larvae show nearly fully penetrant mitochondrial defects in the body wall muscles, including a rounder shape, an "onion"-like crista phenotype and a "vacuole" phenotype. 5 days old adults show a significant decrease in the number of dopaminergic PPL1 neurons, but not of PPL2 neurons, and show a significant decrease in mitochondrial membrane potential. These mutants are flightless and show other locomotor impairments (e.g. crawling in larvae, climbing and jumping in adults).
Pink1B9 mutant adults show significant loss of brain dopaminergic neurons from the PPL1 cluster compared to controls.
Pink1B9 mutant adults display abnormal wing posture, thoracic indentations, climbing and flight deficit along with severe muscle fiber disorganization and aberrant mitochondrial morphology with sparse cristae in the indirect flight muscles. The brain of aged Pink1B9 adults contains fewer dorsolateral 1 (DL1) dopaminergic (da) neurons (but numbers of dorsomedial and posteromedial da neurons is comparable to controls) and da neurons from the PPL1 cluster frequently contain enlarged (aggregated) mitochondria.
Young Pink1B9 mutants display significant impairment in 2min memory in an olfactory memory aversive assay (but do not show any smell perception defects) compared to wild-type controls. The mutants also show relatively normal circadian locomotor activity rhythm in LD (light-dark) and while majority of Pink1B9 flies are totally arrhythmic some maintain discernible activity rhythmicity in DD (constant dark) but there is less of a distinction between periods of activity and inactivity and their relative night-time activity appears elevated. Aging does not affect the circadian rhythm of Pink1B9 any more than in wild-type controls. Like in wild-type, the l-LNv neurons in Pink1B9 mutants show a day/night difference in spontaneous firing rate (SFR) and comparable resting membrane potentials, but the mutants have higher SFR, especially in the daytime, and are more excitable and fire more frequently in response to injected current.
Pink1B9 homozygous mutant adults present a significant decrease in lifespan, a significant decrease in the climbing capacity and a defective thorax in the majority of cases; their adult brains also present a significant decrease in the number of dopaminergic PPL1 neurons and severe mitochondria defects, as shown by a significant decrease in mitochondrial potential as compared to controls and fragmented mitochondria cristae in adult brain neuropils.
Pink1B9 homozygotes exhibit a significant increase in the proportion of hyperplastic testes as compared to controls.
Pink1B9 mutants adults show locomotor deficit (reduced climbing ability) as well loss of dopaminergic neurons from the dorsolateral cluster 1.
Pink1B9 mutants show significantly increased number of mitochondria-endoplasmic reticulum contacts in the adult brain compared to controls.
When placed on medium containing rotenone, Pink1B9/Pink1B9 flies show significantly decreased survival compared to wild type flies. Pink1B9/Pink1B9 flies have thoracic indentations and downturned wings, show mitochondrial disruption and apoptotic cell death in the indirect flight muscle and adults have locomotor defects (reduced climbing ability) compared to controls. Pink1B9/Pink1B9 30 day old flies show significant dopamine neuron loss, specifically in dorsolateral clusters 1 (DL1) and dorsomedial clusters (DM). Pink1B9/Pink1B9 flies fed food containing gamitrinib-triphenylphosphonium (G-TPP) show significant dose-dependent rescue of locomotor defects (climbing ability); after 30 days of G-TPP administration, loss of dopaminergic neurons (DL1 and DM clusters) in Pink1B9/Pink1B9 flies is also rescued in a dose-dependent manner.
Pink1B9 homozygous adults, but not Pink1B9/Pink1mCherry transheterozygous, adults display near fully penetrant wing posture defects, as compared to Pink1B9 heterozygous controls. Pink1B9 homozygous clones within mosaic midguts present enterocytes with a significantly increased relative mitochondrial content during pupariation, but not at 4 or 6 hours after pupariation, as compared to non-clone enterocytes.
Pink1B9 adult mutants display abnormal swollen mitochondria in indirect flight muscles.
Pink1B9 homozygous adults present locomotion defects, as assessed by negative geotaxis assays, and a significant proportion of the population exhibit a crushed thorax and progressive wing posture defects, which increase in prevalence with age, as compared to controls; these adults also exhibit abnormal aggregation of mitochondria in the thorax, in indirect flight muscles, and in dendritic arborizing neurons, as compared to controls.
Pink1B9 mutant adults show reduced climbing ability, defective mitochondrial morphology in indirect flight muscles and loss of dopaminergic neurons.
Thoracic muscles of Pink1B9/Pink1B9 mutant adults display fragmented mitochondrial cristae.
Pink1B9 homozygote mutant adults display wing posture defects, reduced jumping ability, loss of dopaminergic neurons (DA) from the PPL1 cluster along with mitochondrial aggregations in flight muscles and DA neurons.
Mitochondria are mislocalized and clustered in Pink1B9/Df(1)BSC535 germ cells in the ovary; presence of doughnut-shaped mitochondria suggests clumps may consist of abnormally fused mitochondria. Mitochondria disperse normally in Pink1B9/+ germ cells in the ovary. Pink1B9/y males have abnormal wing posture and thoracic indentations, mitochondrial pattern in flight muscle is grossly disrupted, and mitochondria are swollen and have fragmented inner membranes.
Dietary C18:0 supplementation (10%) significantly increases lifespan of male Pink1B9. Dietary C18:0 supplementation rescues ATP levels of 1-week-old male Pink1B9 mutant adult flies. Dietary C18:0 supplementation significantly improves locomotor defects of 2-week-old male Pink1B9 mutant flies.
Pink1B9 mutant flies show elevated response across a range of spatiotemporal frequencies of contrast-reversing sine-wave gratings as compared to responses from control flies.
Adult Pink1B9 hemizygous males display indentations in the thorax with high penetrance as well as muscle and mitochondria degeneration and their ability to fly is severely copromised. Pink1B9 hemizygous third instar larvae show enlarged or aggregated mitochondria throughout the body wall muscles.
Mitochondria from Pink1B9 indirect flight muscles show defective morphology - disorganized cristae and enlarged size. Pink1B9 flies show poor performance in a climbing assay and depletion of dopamine in the brain.
3-5 day old Pink1B9 mutant flies show indirect flight muscle degeneration. One or several of the six muscles has highly degenerated, highly irregular myofibrils with abnormal sarcomere structure in 65% of the animals as compared to controls. The indirect flight muscles of Pink1B9 mutants display a heterogeneous population of mitochondria with the majority having significantly enlarged sizes and mild or severe disruption of their cristae structure, when compared to control mitochondria. Severely enlarged mitochondria are also seen in dopaminergic neurons. Pink1B9 mutants show reduced ATP content in the thorax to approximately 40% of controls. Complex 1 activity is markedly reduced.
Pink1B9 mutant flies fail to maintain neurotransmitter release at neuromuscular junctions during high frequency stimulations (10Hz). Reserve pool vesicle loading is disrupted and there is a decrease in mitochondrial membrane potential at NMJ boutons. ATP content is decreased. Severe muscle degeneration and flight defects are also seen in Pink1B9 mutant flies, with mitochondrial morphology defects in the flight muscles.
Pink1B9/Pink1B9 flies have a short lifespan, and display mitochondrial aggregation, muscle degeneration, and wing posture abnormalities, but do not display dopaminergic neuron loss at 35-days old, as compared to controls.
Pink1B9 mutant flies display a significantly shorter lifespan with respect to wild type flies. Feeding the flies 0.1% Mucuna pruriens extract (Mpe) during the larval and adult stages significantly increases lifespan. This effect is not seen when the Mpe is given only during the adult stages, or when the concentration is increased to 1% or 10%. Treatment with 0.01% L-Dopa throughout the larval and adult stages has no effect. Pink1B9 mutant flies exhibit impaired climbing behavior that worsens with age. Feeding the flies 0.1% Mucuna pruriens extract (Mpe) significantly ameliorates the climbing activity and reduces the worsening trend with aging. Treatment with 1% Mpe ameliorates climbing defects only at early ages and 10% fails to ameliorate defects are two out of three timepoints. L-Dopa treatment has no effect at most time points, with the number of flies able to complete the task worsening over time. The average EAG signal amplitude stimulated by 1-hexanol is significantly lower in Pink1B9 flies with respect to wild type and this is partially rescues when the flies are fed either 0.1% Mucuna pruriens extract (Mpe) or 0.01% L-Dopa. Olfactory behavior in response to 1-hexanol is also impaired in Pink1B9 mutants and feeding the flies either 0.1% Mpe or 0.01% L-Dopa rescues this phenotype. A similar impairment of olfactory behavior is seen in Pink1B9 mutant flies in response to water. A significant decrease in T-bar density is observed in the presynaptic bouton active zones of both antennal lobes and thoracic ganglia of Pink1B9 mutants with respect to wild type controls. Feeding the flies 0.1% Mucuna pruriens extract (Mpe) partially suppresses this reduction. The number of damaged, swollen and mitochondria with clearly fragmented cristae is significantly lower in presynaptic boutons of antennal lobes of Mpe-treated Pink1B9 mutants compared to untreated mutants.
Pink1B9 adult mutants are short lived compared to controls.
Mutant flies show a reduction in the mtDNA/nDNA ratio compared to controls. Mutant flies show mitochondrial defects in the indirect flight muscles. These defects are reduced if the flies are raised on a diet supplemented with either deoxyribonucleosides or folate. Mutant flies show a loss of mitochondrial mass and mitochondrial potential in the brain. Mutant adults show loss of dopaminergic neurons in the PPL1 cluster. Mutant adults often have thoracic defects and show reduced flight ability. These defects are reduced if the flies are raised on a diet supplemented with either deoxyribonucleosides or folate.
Pink1B9/Pink1B9 flies have a crushed thorax (significantly increased percentage of thoracic indentations), locomotor defects (significantly slower climbing), male sterility, degeneration (cell death) and disorganization and fewer mitochondrial cristae in indirect flight muscle, disorganized spermatids, distorted and vacuolated nebenkerns, defects in mitochondrial morphology, mitochondrial loss and dopaminergic neuron loss (especially DL1 cluster) compared to wild type. Paraquat or rotenone-induced lethality is enhanced in Pink1B9/Pink1B9 flies compared to wild type.
10 day old mutant flies have impaired climbing ability compared to controls. Mutant flies have thoracic indentations.
The flight muscles of mutant adults have swollen mitochondria. Dopaminergic neurons in the adult brain contain mitochondrial aggregates. Mutant mitochondrial preparations produce higher levels of O[[2]][-] (superoxide) than wild-type mitochondria and contain higher levels of Fe[2+] than wild type. The mutant flies show increased levels of H[[2]]O[[2]] and its derivatives compared to wild type.
Mutant adults often have a collapsed thorax phenotype. The flight muscles of 3 day old adults show an increase in apoptotic cell death compared to controls. 1 day old mutant adults have a normal number of dopaminergic (DA) neurons in the PPL1 cluster of the brain. However, the number of DA neurons in the PPL1 cluster is decreased by 20% compared to controls in 20 day old mutant adults.
Most Pink1B9 adults have indentations in the dorsal thorax. Mutant adults show reduced climbing ability compared to controls.
Mutant flies have an abnormal wing posture, with the fraction of flies affected increasing with age.
Mutant flies have a reduced lifespan compared to controls. The flies start to die dramatically about 15 days after eclosion. Maximum lifespan is approximately 53 days. 3 to 6 day old flies show a significantly reduced electroantennogram (EAG) amplitude compared to wild type in response to one of the essential oils rosemary, lentisk or myrtle or one of the synthetic compounds 1-hexanol or α-pinene at concentrations of 1% and 10%. Similar to wild type, the EAG response is dose sensitive. Both mutant and wild-type flies show a progressive decrease in olfactory response with age, with the mutant flies showing a reduced response compared to age-matched controls at both 15-20 and 27-30 days of age. The antennal lobes of mutant adult brains show no significant difference in volume from wild-type controls. The mitochondria within the presynaptic boutons of mutant antennal lobes appear degenerated compared to those of wild-type controls, being swollen and often having wide swellings on the outer membrane. The mitochondrial cristae are ether clearly fragmented or completely deteriorated and appear to be surrounded by a highly altered, inhomogeneous electron transparent mitochondrial matrix. The number of presynaptic boutons without mitochondria is significantly increased compared to wild type. Mutant flies do not show a significant difference to wild type in free-walking bioassays of olfactory behaviour.
Pink1B9 mutant flies exhibit crushed thoraces and downturned wings. The thoracic muscles contain swollen or enlarged mitochondria between disorganised muscle fibres, ATP levels are markedly reduced compared to control flies and the mutants are unable to fly. These phenotypes are seen in both three day and 45 day old flies. Pink1B9 mutant flies also show reduced numbers of dopaminergic neurons in dorsolateral region 1.
Compared with wild-type, the flight ability of 5-day old Pink1B9 mutants is impaired. Near infrared 808 nm light irradiation results in improved flight ability of the mutants, while no effect is observed in control flies. Pink1B9 mutant flies suffer from mitochondrial dysfunction. 808 nm light irradiation rescues the mitochondrial functional defect in Pink1B9 mutants. Light stimulation also significantly decreases the number of aggregated and swollen mitochondria in the mutants, but has no detectable effect on mitochondrial morphology.
Mutants show mitochondrial aggregation in dopaminergic neurons. Mutant flies show loss of dopaminergic neurons in the PPL1 cluster.
Pink1B9 mutant males display a 40% reduction in levels of germline cell death in spermatogonial cysts.
Hemizygous flies often have an abnormal wing posture. Indentations in the thorax are also seen. Climbing index and flight ability are reduced compared to wild type. Indirect flight muscles show vacuolisation in 5 day old Pink1B9/Y flies. The mitochondria in these muscles appear swollen and have disrupted cristae.
Mutant adults show an indented thorax phenotype and have reduced climbing ability compared to controls. Mitochondrial clustering is seen in the indirect flight muscles. Loss of dopaminergic neurons in the PPL1 cluster is seen.
Pink1B9 flies are sensitive to heat shock stress and die sooner than control flies.
Pink1B9/Y flies have a collapsed thorax phenotype, downturned wings, swollen mitochondria and signs of cell death in the indirect flight muscle (and levels of mtDNA and ATP are reduced), and show significant locomotor defects (reduced climbing ability) compared to controls. Mitochondria are enlarged in dopaminergic neurons of 3 day old Pink1B9/Y flies and there is a significant decrease in dopaminergic neuron number (especially in the DL1 cluster) in 30 day old flies.
Pink1B9/Pink1B9 mutant adults display abnormal wing posture and decreased flight activity, increasing with age; dopaminergic neuron loss, and mitochondrial aggregation in dopaminergic neurons.
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 flies show a significant reduction in O[[2]] consumption for both Complex-I and Complex-IV driven respiration compared to wild type. Mitochondria show a severe deficit in ATP synthesis compared to wild type.
Mutant adults show defects in climbing and flight ability and have thoracic indentations.
Pink1B9/Pink1B9 mutants display abnormal wing posture in a majority of 6 day old flies, thoracic muscle defects with presence of abnormal vacuoles, and muscle apoptosis as seen with TUNEL staining.
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.
Pink1B9 mutant adults show age-progressive decline in climbing abilities.
The amplitude of the excitatory junctional potential (EJP) at the neuromuscular junction (NMJ) is normal in mutant third instar larvae. Spontaneous mEJP amplitude and frequency measured in 0.5mM Ca[2+] in the presence of tetrodotoxin are also normal. However, when stimulated at 10Hz, EJP amplitudes at the mutant NMJ show a small but progressive decline over time. Defects in mobilisation of the reserve pool of synaptic vesicles are seen in the mutants. No significant defects in mitochondrial morphology are seen at the NMJ in mutant third instar larvae. Mitochondrial membrane potential at the mutant NMJ is reduced in mutant flies compared to controls. NMJ length/muscle area and bouton number/muscle area are not significantly different from wild type at the mutant NMJ.
Mutant flies have a downturned wing position and crushed thorax and are flightless. Mutants have unusually large swollen mitochondria in the dopaminergic neurons.
Pink1B9/Pink1B9 flies have significant defects in climbing and flight ability, as well as muscle degeneration and mitochondrial disruption, compared to heterozygotes; 30 day old mutants show significant loss of dopaminergic PPL1 neurons. Pink1B9/Pink1B9 flies have significant indentations in the thorax (indications of flight muscle degeneration).
Pink1B9 hemizygous mutants display thoracic indentations, impaired flight ability, climbing defects, and mitochondrial morphological defects.
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 Pink1B9 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.
External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference
Pink1B9 has increased mortality | chemical conditional phenotype, enhanceable by Ucp4ADL/Ucp4ADL
Pink1B9 has flight defective phenotype, enhanceable by heix[+]/heix1
Pink1B9 has flight defective phenotype, enhanceable by heix2/heix[+]
Pink1B9 has flight defective phenotype, enhanceable by heixk11403/heix[+]
Pink1B9 has flight defective phenotype, enhanceable by heix[+]/heixNP5301
Pink1B9 has visible phenotype, enhanceable by Df(2L)BSC50/+
Pink1B9 has visible phenotype, enhanceable by Df(2R)nap9/+
Pink1B9 has visible phenotype, enhanceable by Df(2R)cn9/+
Pink1B9 has visible phenotype, enhanceable by Df(2R)BSC39/+
Pink1B9 has visible phenotype, enhanceable by +/Df(3R)BSC47
NOT Enhanced by
Statement
Reference
Pink1B9 has visible phenotype, non-enhanceable by Df(3R)Tpl10/+
Suppressed by
Statement
Reference
Pink1B9 has decreased cell number | adult stage phenotype, suppressible by Parp[+]/ParpCH1
Pink1B9 has short lived phenotype, suppressible | partially by Parp[+]/ParpCH1
Pink1B9 has neuroanatomy defective | adult stage phenotype, suppressible by Parp[+]/ParpCH1
Pink1B9 has oxidative stress response defective | adult stage | chemical conditional phenotype, suppressible by Trap1D6/Trap1D6
Pink1B9 has visible phenotype, suppressible | partially by Trap1D6/Trap1D6
Pink1B9 has oxidative stress response defective | adult stage | chemical conditional phenotype, suppressible by Trap1EY21851/Trap1EY21851
Pink1B9 has flight defective phenotype, suppressible | partially by mask[+]/mask10.22
Pink1B9 has flight defective phenotype, suppressible | partially by mAcon11/Acon[+]
Pink1B9 has flight defective phenotype, suppressible | partially by mAcon1MB09176/Acon[+]
Pink1B9 has flight defective phenotype, suppressible | partially by mAcon11/Drp1+t9.4/Acon[+]
Pink1B9 has visible phenotype, suppressible by Df(2L)BSC106/+
Pink1B9 has visible phenotype, suppressible by Df(2L)BSC109/+
Pink1B9 has visible phenotype, suppressible by Df(2L)BSC142/+
Pink1B9 has visible phenotype, suppressible by Df(2R)Exel7131/+
Pink1B9 has visible phenotype, suppressible by Df(2R)P34/+
Pink1B9 has visible phenotype, suppressible by Df(3L)XDI98/+
Pink1B9 has visible phenotype, suppressible by Df(3L)BSC33/+
Pink1B9 has visible phenotype, suppressible by Df(3L)Scf-R6/+
Pink1B9 has visible phenotype, suppressible by +/Df(3L)BSC10
Pink1B9 has visible phenotype, suppressible by Df(3R)p-XT103/+
Pink1B9 has visible phenotype, suppressible by Df(3R)P115/+
Pink1B9 has visible phenotype, suppressible by Df(3R)Exel6203/+
Pink1B9 has visible phenotype, suppressible by Pgam5NP0568
Pink1B9 has short lived phenotype, suppressible by Pgam5NP0568
Pink1B9 has visible phenotype, suppressible by Pgam51
Pink1B9 has short lived phenotype, suppressible by Pgam51
Pink1B9 has visible phenotype, suppressible by opa1-like[+]/Opa1EY09863
Pink1B9 has visible phenotype, suppressible | partially by Opa1[+]/Opa1f02779
Pink1B9 has flight defective phenotype, suppressible | partially by Opa1[+]/Opa1f02779
Pink1B9 has visible phenotype, suppressible | partially by Opa1[+]/Opa1s3475
Pink1B9 has flight defective phenotype, suppressible | partially by Opa1[+]/Opa1s3475
Pink1B9 has visible phenotype, suppressible | partially by Drp1+t9.4
NOT suppressed by
Statement
Reference
Pink1B9 has visible | progressive phenotype, non-suppressible by NGD14477/Scer\GAL4Mhc.PW
Pink1B9 has visible | progressive phenotype, non-suppressible by Scer\GAL4Mhc.PW/NGD144
Pink1B9 has male sterile phenotype, non-suppressible by Drp1+t9.4
Pink1B9 has male sterile phenotype, non-suppressible by Opa1s3475
Pink1B9 has visible phenotype, non-suppressible by +/Df(2L)dp-79b
Pink1B9 has visible phenotype, non-suppressible by Df(2L)BSC143/+
Pink1B9 has visible phenotype, non-suppressible by Df(2R)BSC550/+
Pink1B9 has visible phenotype, non-suppressible by Df(3L)66C-G28/+
Pink1B9 has visible phenotype, non-suppressible by Df(3L)ME107/+
Pink1B9 has visible phenotype, non-suppressible by Df(3R)crb-F89-4/+
Pink1B9 has visible phenotype, non-suppressible by Df(3R)Exel6202/+
Pink1B9 has visible phenotype, non-suppressible by Scer\GAL4da.PU/dj-1βC104A.UAS
Pink1B9 has visible phenotype, non-suppressible by Drp12/Drp1[+]
Pink1B9 has flightless phenotype, non-suppressible by Drp12/Drp1[+]
Pink1B9 has flightless phenotype, non-suppressible by opa1-like[+]/Opa1EY09863
Pink1B9 has locomotor behavior defective phenotype, non-suppressible by park25
Enhancer of
Statement
Reference
NOT Enhancer of
Suppressor of
NOT Suppressor of
Statement
Reference
Other
Statement
Reference
Phenotype Manifest In
Enhanced by
Statement
Reference
Pink1B9 has wing phenotype, enhanceable by Df(2L)BSC50/+
Pink1B9 has wing phenotype, enhanceable by Df(2R)nap9/+
Pink1B9 has wing phenotype, enhanceable by Df(2R)cn9/+
Pink1B9 has wing phenotype, enhanceable by Df(2R)BSC39/+
Pink1B9 has wing phenotype, enhanceable by +/Df(3R)BSC47
NOT Enhanced by
Statement
Reference
Suppressed by
Statement
Reference
Pink1B9 has adult thorax phenotype, suppressible | partially by Parp[+]/ParpCH1
Pink1B9 has adult brain phenotype, suppressible | partially by Parp[+]/ParpCH1
Pink1B9 has neuropil | adult stage phenotype, suppressible | partially by Parp[+]/ParpCH1
Pink1B9 has dopaminergic PPL1 neuron | adult stage phenotype, suppressible by Parp[+]/ParpCH1
Pink1B9 has wing phenotype, suppressible | partially by Trap1D6/Trap1D6
Pink1B9 has wing | progressive phenotype, suppressible by Scer\GAL4Mhc.PU
Pink1B9 has thorax phenotype, suppressible by Scer\GAL4Mhc.PU
Pink1B9 has adult external thorax phenotype, suppressible | partially by mask[+]/mask10.22
Pink1B9 has mitochondrion phenotype, suppressible | partially by mAcon11/Acon[+]
Pink1B9 has mitochondrion phenotype, suppressible | partially by mAcon1MB09176/Acon[+]
Pink1B9 has mitochondrion phenotype, suppressible by ref(2)Pod2
Pink1B9 has mitochondrion phenotype, suppressible by ref(2)Pod3
Pink1B9 has wing phenotype, suppressible by Df(2L)BSC106/+
Pink1B9 has wing phenotype, suppressible by Df(2L)BSC109/+
Pink1B9 has wing phenotype, suppressible by Df(2L)BSC142/+
Pink1B9 has wing phenotype, suppressible by Df(2R)Exel7131/+
Pink1B9 has wing phenotype, suppressible by Df(2R)P34/+
Pink1B9 has wing phenotype, suppressible by Df(3L)XDI98/+
Pink1B9 has wing phenotype, suppressible by Df(3L)BSC33/+
Pink1B9 has wing phenotype, suppressible by Df(3L)Scf-R6/+
Pink1B9 has wing phenotype, suppressible by +/Df(3L)BSC10
Pink1B9 has wing phenotype, suppressible by Df(3R)p-XT103/+
Pink1B9 has wing phenotype, suppressible by Df(3R)P115/+
Pink1B9 has wing phenotype, suppressible by Df(3R)Exel6203/+
Pink1B9 has wing phenotype, suppressible by Scer\GAL4da.PU/parkUAS.cGa
Pink1B9 has adult thorax phenotype, suppressible by Pgam5NP0568
Pink1B9 has wing phenotype, suppressible by Pgam5NP0568
Pink1B9 has mitochondrion phenotype, suppressible | partially by Pgam5NP0568
Pink1B9 has adult thorax phenotype, suppressible by Pgam51
Pink1B9 has wing phenotype, suppressible by Pgam51
Pink1B9 has mitochondrion phenotype, suppressible | partially by Pgam51
Pink1B9 has mitochondrion & dopaminergic neuron phenotype, suppressible by Scer\GAL4ple.PF/parkUAS.Tag:MYC/Scer\GAL4ple.PF
Pink1B9 has wing phenotype, suppressible by opa1-like[+]/Opa1EY09863
Pink1B9 has adult thorax phenotype, suppressible by opa1-like[+]/Opa1EY09863
Pink1B9 has mitochondrion & dopaminergic neuron phenotype, suppressible by opa1-like[+]/Opa1EY09863
Pink1B9 has wing phenotype, suppressible by MarfGD11094/Scer\GAL4hs.PB
Pink1B9 has mitochondrion & dopaminergic neuron phenotype, suppressible by Scer\GAL4ple.PF/Drp1UAS.Tag:HA/Scer\GAL4ple.PF
Pink1B9 has adult thorax phenotype, suppressible | partially by Opa1[+]/Opa1f02779
Pink1B9 has adult thorax phenotype, suppressible | partially by Opa1[+]/Opa1s3475
Pink1B9 has mitochondrion phenotype, suppressible | partially by Opa1[+]/Opa1s3475
Pink1B9 has adult thorax phenotype, suppressible | partially by Drp1+t9.4
Pink1B9 has mitochondrion phenotype, suppressible | partially by Drp1+t9.4
Pink1B9 has indirect flight muscle phenotype, suppressible by opa1-like[+]/Opa1EY09863
Pink1B9 has mitochondrion & indirect flight muscle phenotype, suppressible by opa1-like[+]/Opa1EY09863
Pink1B9 has mitochondrial inner membrane & indirect flight muscle phenotype, suppressible by opa1-like[+]/Opa1EY09863
Pink1B9 has mitochondrion & dorso-lateral dopaminergic neuron phenotype, suppressible by opa1-like[+]/Opa1EY09863
Pink1B9 has mitochondrion & indirect flight muscle phenotype, suppressible by Drp1Tag:FLAG,Tag:CALI(TC),Tag:HA
Pink1B9 has mitochondrial inner membrane & indirect flight muscle phenotype, suppressible by Drp1Tag:FLAG,Tag:CALI(TC),Tag:HA
Pink1B9 has mitochondrion & dorso-lateral dopaminergic neuron phenotype, suppressible by Drp1Tag:FLAG,Tag:CALI(TC),Tag:HA
Pink1B9 has mitochondrion & dorso-lateral dopaminergic neuron phenotype, suppressible by parkUAS.Tag:HA/Scer\GAL4ple.PF/Scer\GAL4ple.PF
Pink1B9 has mitochondrion & dopamine neuron & adult brain phenotype, suppressible | partially by Scer\GAL4ple.PF/parkUAS.Tag:MYC/Scer\GAL4ple.PF
Pink1B9 has dopamine neuron & adult brain phenotype, suppressible | partially by parkUAS.Tag:MYC/Scer\GAL4hs.PB
NOT suppressed by
Statement
Reference
Pink1B9 has wing | progressive phenotype, non-suppressible by NGD14477/Scer\GAL4Mhc.PW
Pink1B9 has wing | progressive phenotype, non-suppressible by Scer\GAL4Mhc.PW/NGD144
Pink1B9 has wing phenotype, non-suppressible by +/Df(2L)dp-79b
Pink1B9 has wing phenotype, non-suppressible by Df(2L)BSC143/+
Pink1B9 has wing phenotype, non-suppressible by Df(2R)BSC550/+
Pink1B9 has wing phenotype, non-suppressible by Df(3L)66C-G28/+
Pink1B9 has wing phenotype, non-suppressible by Df(3L)ME107/+
Pink1B9 has wing phenotype, non-suppressible by Df(3R)crb-F89-4/+
Pink1B9 has wing phenotype, non-suppressible by Df(3R)Exel6202/+
Pink1B9 has wing phenotype, non-suppressible by Scer\GAL4da.PU/dj-1βC104A.UAS
Pink1B9 has wing phenotype, non-suppressible by Drp12/Drp1[+]
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 Opa1UAS.Tag:FLAG/Scer\GAL4hs.PB
Enhancer of
Statement
Reference
NOT Enhancer of
Suppressor of
NOT Suppressor of
Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference
The increased lethality of Pink1B9 mutant adults is not significantly worsened by expression of crcKK111018 under the control of Scer\GAL4da.PU in the mutant background but the penetrance of their crushed-thorax phenotype as well as the severity of their climbing ability defects is significantly increased. The lethality and dented thorax phenotype of Pink1B9 mutants is also enhanced upon Scer\GAL4da.PU-driven expression of either Shmt2GD8851 or NmdmcKK102478, expression of NmdmcKK102478 also further worsens their climbing defects. Expression of either Shmt2Scer\UAS.T:Ivir\HA1 or NmdmcScer\UAS.T:Ivir\HA1 (but not Gcn2KK103566 RNAi) driven by Scer\GAL4elav.PU significantly rescues the loss of dopaminergic ppl1 cluster neurons characteristic for Pink1B9 mutant adults.
The abnormal wing posture, thoracic indentations, climbing and flight deficit along with severe muscle fiber disorganization and aberrant mitochondrial morphology in the indirect flight muscles characteristic for Pink1B9 mutant adults are all strongly (or fully) suppressed by Scer\GAL4Mhc.PU-driven expression of STUB1Scer\UAS.cCa. Similarly, expression of STUB1Scer\UAS.cCa if driven by Scer\GAL4ple.PU rescues the loss of dorsolateral 1 dopaminergic neurons (da) as well as the mitochondrial aggregation frequently observed in PPL1 da neurons in Pink1B9 adult brains. In contrast, expression of either STUB1ΔUbox.Scer\UAS or STUB1H246A.P255A.Scer\UAS controlled by Scer\GAL4Mhc.PU cannot rescue either the mitochondrial defects or the reduced climbing ability of Pink1B9 mutants and this climbing deficit is not exacerbated by combination with either STUB1I or STUB1II in homozygous state and the lifespan of the double mutants is not significantly different from the Pink1B9 single mutants.
ParpCH1 heterozygosity leads to a significant suppression of the defects in lifespan, climbing capacity, thorax morphology, number of dopaminergic PPL1 neurons and mitochondria cristae morphology in the neoropil observed in Pink1B9 homozygous mutant adults; ParpCH1 also rescues the decreased mitochodrial potential observed in the brains of Pink1B9 homozygous mutant adults, as assessed by tetramethylrhodamine fluorescence.
Expression of IdhScer\UAS.c.T:Ivir\HA1 cannot rescue either the locomotor deficit (with the Scer\GAL4da.PU driver) or the loss of brain dopaminergic neurons (with Scer\GAL4ple.PF) characteristic for Pink1B9 mutant adult flies.
The increased number of mitochondria-endoplasmic reticulum contacts observed in the brain of adult Pink1B9 mutants is strongly suppressed by expression of MarfKK105681 RNAi under the control of Scer\GAL4elav.PU in the mutant background. Expression of MarfKK105681 under the control of Scer\GAL4da.PU strongly suppresses the 'crushed thorax' phenotype characteristic for Pink1B9 mutant adults. Expression of PEKGD5584 under the control of Scer\GAL4elav.PU significantly rescues the loss of dopaminergic neurons characteristic for adult Pink1B9 mutants.
Pink1B9 suppresses the ability of Scer\GAL4GMR.PF>Atg1Scer\UAS.cSa to suppress age-dependent retinal degeneration (loss of rhabdomeres from photoreceptors) in trpP365/+ flies.
Presence of Trap1D6/Trap1D6 or Trap1EY21851/Trap1EY21851 significantly suppresses decreased survival in response to rotenone, crushed thorax and downturned wing phenotypes, cell death and disrupted mitochondrial function, and locomotor defects seen in Pink1B9/Pink1B9 flies. Trap1D6/Trap1D6 or Trap1EY21851/Trap1EY21851 significantly suppress dopamine neuron (DL1 and DM) loss in Pink1B9/Pink1B9 30 day old flies. foxo21/+ partially suppresses rescue of locomotor defects by Trap1EY21851/Trap1EY21851 in Pink1B9/Pink1B9 flies. Presence of foxo25/foxo21 suppresses rescue via feeding of G-TTP of locomotor defects in Pink1B9/Pink1B9 flies.
The expression of Hsap\BNIP3Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4Mhc.PU fully suppresses the adult locomotive defects, the wing posture defects, the thorax morphology defects and the mitochondrial aggregation defects in both indirect flight muscles and thorax exhibited by Pink1B9 homozygous adults; expression under the control of Scer\GAL4ple.PU also fully suppresses the mitochondria aggregation defects present in dendritic arborization neurons of Pink1B9 homozygous adults.
The abnormal mitochondrial aggregations (observed in flight muscles or dopaminergic neurons), wing posture and jumping ability defects as well as the loss of dopaminergic neurons from the PPL1 cluster characteristic for Pink1B9 adult homozygotes are significantly improved by expression (controlled by either the Scer\GAL4Mhc.PU muscle driver or the Scer\GAL4ple.PF neuronal driver) of any of the following: pumJF02267, Pop2GD12804, AGO1TRiP.cUa, gwdsRNA.Scer\UAS.cUa, DCP1VDRC.cUa, DCP2HMS00115 or glodsRNA.Scer\UAS.cUa whereas expression of Tim8JF01533, Tom40JF02030, or Tom20KK107626 exacerbates the Pink1B9 loss of function phenotypes (or at least does not suppress them). The wing posture and jumping defects as well as the loss of PPL1 neurons can also be enhanced by expression of Tom7KK112286, while no significant effect on these phenotypes is observed with either Tim10KK109413 or Tim13KK108559. Scer\GAL4Mhc.PU-controlled expression of eIF4G1HMS00762 exacerbates the wing posture and jumping defects but Scer\GAL4ple.PF-driven expression of eIF4G1HMS00762 in the Pink1B9 mutant background is lethal. Conversely, the loss of PPL1 neurons and presence of mitochondrial aggregations in DA neurons in Pink1B9 mutants are significantly suppressed by Scer\GAL4ple.PF-driven expression of Tom20Scer\UAS.cGa but not Tom40Scer\UAS.cGa or Tom70Scer\UAS.cGa.
Vps35MH20 Pink1B9 double heterozygotes do not exhibit climbing defects. Vps35E42 Pink1B9 double heterozygotes do not exhibit climbing defects. Expression of Vps35Scer\UAS.cMa under the control of Scer\GAL4da.PU does not suppress the climbing defects seen in Pink1B9 mutant flies. The flight defects seen in Pink1B9 mutants are enhanced.
Mitochondria in germ cells in the ovary disperse normally in Pink1B9/+ or clud08713/+ heterozygotes, but Pink1B9/+;clud08713/+ double heterozygotes show abnormal clustering. Abnormal wing posture, thoracic indentations, disruption of mitochondrial pattern in flight muscle and swollen mitochondria with fragmented inner membranes seen in Pink1B9/y males are partially suppressed by expression of cluScer\UAS.P\T.cSa driven by Scer\GAL4DJ667. Thoracic indentations seen in Pink1B9/y males are partially suppressed by expression of cluScer\UAS.P\T.cSa driven by Scer\GAL4Mhc.PW.
The indentations on the thorax of adult males hemizygous for Pink1B9 as well as their reduced ability to fly can be partially suppressed, in a dose-dependent manner, by combination with mask10.22/+ or mask10.22/maskEY13048 alleles, which leads to significantly lower penetrance of the thoracic phenotype and increased flight ability compared to Pink1B9 mutants alone. The disturbed morphology of both mitochondria and indirect flight muscles characteristic for adult Pink1B9 hemizygote males is substantially suppressed by combination with mask10.22/+ or mask10.22/maskEY13048 alleles. The enlarged or aggregated mitochondria phenotype observed in the body wall muscles of Pink1B9 hemizygous male third instar larvae is suppressed either by combination with mask10.22/maskEY13048 alleles or by ectopic expression of parkScer\UAS.cGa under the control of Scer\GAL4how-24B. The enlarged or aggregated mitochondria phenotype observed in the body wall muscles of Pink1B9 hemizygous male third instar larvae is suppressed by expression of either maskHMS01045 or maskKK100529 under the control of Scer\GAL4how-24B.
Scer\GAL4Act5C.PI-mediated expression of USP30NIG.3016R largely restores the Pink1B9 mitochondrial morphology defects. Scer\GAL4Act5C.PI-mediated expression of USP30NIG.3016R ameliorates the climbing defect and prevents the dopamine depletion seen in Pink1B9 flies.
Expression of RetMEN2B.Scer\UAS under the control of Scer\GAL4Mef2.PR partially suppresses the muscle morphology phenotype seen in the indirect flight muscles of Pink1B9 mutants. The frequency of flies with "actin blobs" is also decreased markedly compared to RetMEN2B.Scer\UAS expressing controls. The fraction of severely impaired mitochondria is decreased and the fraction of mitochondria with wild type-like cristae is increased. The reduction in thoracic ATP levels is largely rescued, as is the reduction in Complex 1 activity. Expression of RetMEN2B.Scer\UAS under the control of Scer\GAL4Mhc.PK (limited to the pharate adult stages onwards using Scer\GAL80ts.αTub84B) largely suppresses the muscle morphology phenotype seen in the indirect flight muscles of Pink1B9 mutants. Expression of RetMEN2B.Scer\UAS under the control of Scer\GAL4ple.PF suppresses the mitochondrial morphology defects seen in Pink1B9 mutant dopaminergic neurons.
Expression of ND-42SD.Scer\UAS under the control of Scer\GAL4da.PU rescues the defects in NMJ neurotransmitter release seen in Pink1B9 mutant flies. Basal neurotransmitter release is unaffected in these flies. The defect in reserve pool vesicle loading is also rescued, as are the decrease in mitochondrial membrane potential at NMJ boutons and decreased ATP content. However, expression of ND-42SD.Scer\UAS does not rescue the severe flight muscle degeneration and flight defects seen in Pink1B9 mutant flies. Cristae structural organisation is improved without rescuing overall mitochondrial morphology. Expression of ND-42Scer\UAS.cMa under the control of Scer\GAL4da.PU does not rescue the defects in NMJ neurotransmitter release seen in Pink1B9 mutants. Basal neurotransmitter release is unaffected in these flies. The defect in reserve pool vesicle loading, decrease in mitochondrial membrane potential at NMJ boutons and decreased ATP content are also not rescued and there is no improvement in the structural organisation of the mitochondrial cristae in the flight muscles. Expression of ND-42SA.Scer\UAS under the control of Scer\GAL4da.PU does not rescue the defects in NMJ neurotransmitter release seen in Pink1B9 mutant flies. Basal neurotransmitter release is unaffected in these flies. The defect in reserve pool vesicle loading, decrease in mitochondrial membrane potential at NMJ boutons and decreased ATP content are also not rescued and there is no improvement in the structural organisation of the mitochondrial cristae in the flight muscles.
Ubiquitous expression of ND-42Scer\UAS.cBa under the control of Scer\GAL4da.PU restores climbing and flight ability in Pink1B9 mutant flies. Flight muscle and mitochondrial integrity are only partially restored. Male sterility is not improved. Expression of ND-42Scer\UAS.cBa under the control of Scer\GAL4da.PU rescues the reduction in complex I and ATP levels seen in Pink1B9 mutant flies. Ubiquitous expression of ND-42Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4da.PU restores climbing and flight ability in Pink1B9 mutant flies. Ubiquitous expression of sicilyScer\UAS.cZa under the control of Scer\GAL4da.PU restores climbing and flight ability in Pink1B9 mutant flies. Flight muscle and mitochondrial integrity are only partially restored. Expression of sicilyScer\UAS.cZa under the control of Scer\GAL4da.PU rescues the reduction in complex I seen in Pink1B9 mutant flies, but ATP levels are not significantly increased. Ubiquitous expression of ND-42Scer\UAS.cMa under the control of Scer\GAL4da.PU partially rescues the climbing defects seen in Pink1B9 mutant flies. The flight defects are not significantly rescued. Expression of ND-42Scer\UAS.cMa under the control of Scer\GAL4da.PU rescues the reduction in complex I seen in Pink1B9 mutant flies. Ubiquitous expression of ND-42SA.Scer\UAS under the control of Scer\GAL4da.PU partially rescues the climbing and flight defects seen in Pink1B9 mutant flies. The flight defects are not significantly rescued. Expression of ND-42SA.Scer\UAS under the control of Scer\GAL4da.PU rescues the reduction in complex I seen in Pink1B9 mutant flies. Ubiquitous expression of ND-42SD.Scer\UAS under the control of Scer\GAL4da.PU partially rescues the climbing and flight defects seen in Pink1B9 mutant flies. Expression of ND-42SD.Scer\UAS under the control of Scer\GAL4da.PU rescues the reduction in complex I seen in Pink1B9 mutant flies. Ubiquitous expression of parkScer\UAS.cGa under the control of Scer\GAL4da.PU restores climbing and flight ability in Pink1B9 mutant flies. Expression of parkScer\UAS.cGa under the control of Scer\GAL4da.PU rescues the reduction in ATP level seen in Pink1B9 mutant flies, but complex I activity is not significantly increased.
The abnormally large, fused mitochondria observed in Pink1B9 mutant flies are completely rescued when parkSA.Scer\UAS is expressed under the control of Scer\GAL4Mhc.PU. The abnormally large, fused mitochondria observed in Pink1B9 mutant flies are completely rescued when parkScer\UAS.cSa is expressed under the control of Scer\GAL4Mhc.PU. Expression of parkScer\UAS.cSa under the control of Scer\GAL4Mhc.PU suppresses the reduction in ATP levels seen in Pink1B9 mutant flies. The reduction in climbing ability and wing and thorax defects are also rescued. Expression of parkScer\UAS.cSa under the control of Scer\GAL4ple.PU in a Pink1B9 mutant background rescues the mitochondrial aggregation and distribution defects seen with either mutation alone. Expression of parkSE.Scer\UAS under the control of Scer\GAL4Mhc.PU in a Pink1B9 mutant background results in reduced ATP levels compared to expression of parkSE.Scer\UAS or Pink1B9 alone. Expression of parkSE.Scer\UAS under the control of Scer\GAL4Mhc.PU fails to suppress the climbing defects seen in Pink1B9 mutant flies. Pink1B9 partially suppresses the abnormal wing posture seen in flies expressing parkSE.Scer\UAS under the control of Scer\GAL4Mhc.PU. Expression of parkSA.Scer\UAS under the control of Scer\GAL4Mhc.PU suppresses the reduction in ATP levels seen in Pink1B9 mutant flies. The reduction in climbing ability and wing and thorax defects are also rescued. Expression of parkSA.Scer\UAS under the control of Scer\GAL4ple.PU rescues the mitochondrial aggregation and distribution defects seen in Pink1B9 mutant dopaminergic neurons. Pink1B9 does not suppress the mitochondria defects seen when parkSE.Scer\UAS is expressed under the control of Scer\GAL4ple.PU. Pink1B9 partially suppresses the dopaminergic neuron loss seen when parkScer\UAS.cSa is expressed under the control of Scer\GAL4ple.PU. Pink1B9 does not suppress the dopaminergic neuron loss seen when parkSE.Scer\UAS is expressed under the control of Scer\GAL4ple.PU. Pink1B9 enhances the dopaminergic neuron loss seen when parkSA.Scer\UAS is expressed under the control of Scer\GAL4ple.PU.
Expression of dnkScer\UAS.cLa under the control of Scer\GAL4da.PU suppresses the reduction in the mtDNA/nDNA ratio seen in Pink1B9 flies. Mitochondrial defects in the indirect flight muscles are rescued. Expression of dnkScer\UAS.cLa under the control of Scer\GAL4elav.PU suppresses the loss of dopaminergic neurons in the PPL1 cluster which is seen in Pink1B9 flies. The loss of mitochondrial mass and mitochondrial potential in the brain is also suppressed. The adult thorax defects are suppressed.
Overexpression of Ucp4AScer\UAS.cWa (but not Ucp4BScer\UAS.cWa or Ucp4CScer\UAS.cWa) with Scer\GAL4tub.PU reduces thoracic indentations and locomotor defects in Pink1B9/Pink1B9 flies. Overexpression of Ucp4AScer\UAS.cWa with Scer\GAL4tub.PU rescues cell death and disorganisation and fewer mitochondrial cristae within the indirect flight muscle, along with restoring morphology and organization of spermatids and mitochondria, and suppressing reduction of dopaminergic neurons in Pink1B9/Pink1B9 flies. Overexpression of Ucp4AScer\UAS.cWa with Scer\GAL4tub.PU rescues (Ucp4BScer\UAS.cWa or Ucp4CScer\UAS.cWa partially rescues) male sterility in Pink1B9/Pink1B9 flies. Pink1B9/Pink1B9 Ucp4ADL/Ucp4ADL double mutants have significantly shorter life spans in the presence of paraquat or rotenone compared to Pink1B9/Pink1B9 flies.
Expression of Trap1Scer\UAS.cCa under the control of either Scer\GAL4da.G32 or Scer\GAL4elav.PU partially suppresses the thoracic indentation phenotype which is seen in Pink1B9 flies. Expression of Trap1Scer\UAS.cCa under the control of Scer\GAL4da.G32 in Pink1B9 flies improves their climbing ability, lifespan, resistance to paraquat and mitochondrial function. Expression of Trap1Scer\UAS.cCa under the control of Scer\GAL4elav.PU improves climbing ability and mitochondrial respiration in Pink1B9 flies.
The mitochondrial morphology defects seen in Pink1B9 adult flight muscles and dopaminergic neurons are significantly suppressed by either Acon1/+ or AconMB09176/+. The flight defects of Pink1B9 adults are also significantly rescued. Expression of Fer3HCHScer\UAS.cMa under the control of Scer\GAL4ple.PF significantly rescues the defects in mitochondrial morphology which are seen in the dopaminergic neurons in Pink1B9 adults. Pink1B9 ; Acon1/+ ; Drp1+t9.4/+ animals show increased flight ability compared to either Pink1B9 ; Acon1/+ or Pink1B9 ; Drp1+t9.4/+ animals. Pink1B9 ; AconMB09176/+ ; Drp1+t9.4/+ animals show increased flight ability compared to either Pink1B9 ; AconMB09176/+ or Pink1B9 ; Drp1+t9.4/+ animals.
Expression of GstO2A.Scer\UAS under the control of Scer\GAL4Mef2.PU significantly decreases the penetrance of the collapsed thorax phenotype seen in Pink1B9 adults. The increased cell death seen in the flight muscles of 3 day old Pink1B9 adults is also suppressed. The loss of dopaminergic neurons in the PPL1 cluster of the brain which is seen in 20 day old Pink1B9 flies is significantly suppressed by expression of GstO2A.Scer\UAS under the control of Scer\GAL4ple.PF.
Expression of TER94Scer\UAS.cRa under the control of Scer\GAL4EDTP-DJ694 partially suppresses the thorax indentation phenotype and climbing defects seen in Pink1B9 adults. The mitochondrial defects seen in the flight muscles of Pink1B9 adults are suppressed by expression of TER94Scer\UAS.cRa under the control of Scer\GAL4EDTP-DJ694.
Expression of NScer\UAS.T:SV5\V5,T:Zzzz\His6 under the control of Scer\GAL4Mhc.PW suppresses the abnormal wing posture of Pink1B9 flies.
The mitochondrial aggregation phenotype seen in the dopaminergic neurons of Pink1B9 flies is strongly suppressed by expression of rictorScer\UAS.cHa under the control of Scer\GAL4ple.PF and moderately suppressed by co-expression of Sin1Scer\UAS.T:Zzzz\FLAG under the control of Scer\GAL4ple.PF. The mitochondrial aggregation phenotype seen in the dopaminergic neurons of Pink1B9 flies is enhanced by expression of rictorJF01370 under the control of Scer\GAL4ple.PF. The loss of dopaminergic neurons in the PPL1 cluster seen in Pink1B9 flies is suppressed by expression of either rictorScer\UAS.cHa or Sin1Scer\UAS.T:Zzzz\FLAG under the control of Scer\GAL4ple.PF. The loss of dopaminergic neurons in the PPL1 cluster seen in Pink1B9 flies is enhanced by expression of rictorJF01370 under the control of Scer\GAL4ple.PF. The mitochondrial aggregation phenotype seen in the dopaminergic neurons of Pink1B9 flies is suppressed by expression of either trcL.Scer\UAS or trcS292E.Scer\UAS under the control of Scer\GAL4ple.PF. The mitochondrial aggregation phenotype seen in the dopaminergic neurons of Pink1B9 flies is enhanced by expression of trcK122A+T453A.Scer\UAS under the control of Scer\GAL4ple.PF. The loss of dopaminergic neurons in the PPL1 cluster seen in Pink1B9 flies is suppressed by expression of either trcL.Scer\UAS or trcS292E.Scer\UAS under the control of Scer\GAL4ple.PF. The loss of dopaminergic neurons in the PPL1 cluster seen in Pink1B9 flies is enhanced by expression of trcK122A+T453A.Scer\UAS under the control of Scer\GAL4ple.PF.
Expression of ref(2)PScer\UAS.T:Ivir\HA1 under the control of either Scer\GAL4da.G32 or Scer\GAL4elav.PU significantly suppresses the penetrance of the indented thorax phenotype seen in Pink1B9 mutants. Expression of ref(2)PScer\UAS.T:Ivir\HA1 under the control of Scer\GAL4da.G32 suppresses the reduced climbing ability of Pink1B9 adults. Indirect flight muscles show improved tissue structure and mitochondrial integrity compared to Pink1B9 single mutants. Expression of ref(2)PScer\UAS.T:Ivir\HA1 under the control of Scer\GAL4elav.PU suppresses the loss of dopaminergic neurons in the PPL1 cluster which is seen in Pink1B9 mutants. The mitochondrial clustering seen in the indirect flight muscles of Pink1B9 flies is significantly suppressed by each of ref(2)Pod2 and ref(2)Pod3. Expression of parkScer\UAS.cGa under the control of Scer\GAL4da.G32 significantly suppresses the penetrance of the indented thorax phenotype seen in Pink1B9 mutants. This suppression is reduced if the flies are also carrying either ref(2)Pod2 or ref(2)Pod3. The ability of parkScer\UAS.cGa expressed under the control of Scer\GAL4da.G32 to suppress the Pink1B9 mutant phenotypes of an indented thorax and reduced climbing ability is suppressed if the flies are also mutant for Atg1Δ3D. The ability of ref(2)PScer\UAS.T:Ivir\HA1 expressed under the control of Scer\GAL4da.G32 to suppress the Pink1B9 mutant phenotypes of an indented thorax and reduced climbing ability is suppressed if the flies are also mutant for Atg1Δ3D.
Pgam51 Pink1B9 double mutant flies are more sensitive to heat shock stress than either single mutant alone.
Pink1B9/Y does not enhance eye phenotypes seen in Scer\GAL4ey.PU>Sirt1Scer\UAS.cGa flies. Expression of Sirt1Scer\UAS.cGa driven by Scer\GAL4arm.PU partially suppresses phenotypes (collapsed thorax, downturned wings, swollen mitochondria along with increased cell death and reduced levels of mtDNA and ATP in the indirect flight muscle and locomotor defects) seen in (3 day old) Pink1B9/Y flies. Presence of foxo25/foxo21 almost completely nullifies the suppressive effect of Scer\GAL4arm.PU>Sirt1Scer\UAS.cGa on phenotypes in Pink1B9/Y flies. foxo25/foxo21 does not significantly enhance phenotypes (collapsed thorax, downturned wings, swollen mitochondria along with increased cell death and reduced levels of mtDNA and ATP in the indirect flight muscle and locomotor defects) seen in Pink1B9/Y flies. Expression of foxoScer\UAS.cKd driven by Scer\GAL4hs.PU partially suppresses phenotypes (collapsed thorax, downturned wings, swollen mitochondria along with increased cell death and reduced levels of mtDNA and ATP in the indirect flight muscle and locomotor defects) seen in (3 day old) Pink1B9/Y flies. Expression of Sod2Scer\UAS.cUa or ThorScer\UAS.cMa driven by Scer\GAL4hs.PU partially suppresses phenotypes (collapsed thorax, downturned wings, reduced levels of mtDNA and ATP in the indirect flight muscle, and locomotor defects) seen in Pink1B9/Y flies. Expression of Sod2Scer\UAS.cUa or ThorScer\UAS.cMa driven by Scer\GAL4ple.PF partially suppresses the enlarged mitochondria in dopaminergic neurons and dopaminergic neuron loss (DL1 cluster) seen in Pink1B9/Y flies. Expression of Sirt1EP2300 driven by Scer\GAL4ple.PF suppresses the enlarged mitochondria in dopaminergic neurons and dopaminergic neuron loss (DL1 cluster) seen in Pink1B9/Y flies; additional presence of foxo21/+ partially suppresses the suppressive effect of Sirt1EP2300 driven by Scer\GAL4ple.PF on these phenotypes in Pink1B9/Y flies.
Expression of MiroKK102189, MiroJF02775, miltJF03022 or KhcJF01939 under the control of Scer\GAL4Mhc.PU partially rescues the abnormal wing posture and flight defects of Pink1B9/Pink1B9 mutants. Expression of MiroScer\UAS.cGa or Khc248-2134.Scer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4Mhc.PU enhances the abnormal wing posture and flight defects of Pink1B9/Pink1B9 mutants. Expression of MiroKK102189 under the control of Scer\GAL4ple.PF rescues the dopaminergic neuron loss and mitochondrial aggregation phenotypes of Pink1B9/Pink1B9 mutants. Expression of MiroScer\UAS.cGa under the control of Scer\GAL4ple.PF in a Pink1B9/Pink1B9 mutant background does not result in a significant difference in dopaminergic neuron number as compared to in a wild-type background, but does result in reduced viability.
The mitochondrial morphology defects of Pink1B9 larvae are partially rescued by expression of heixScer\UAS.cVa under the control of Scer\GAL4da.G32.
Expression of parkScer\UAS.cGa, but not dj-1βC104A.Scer\UAS, under the control of Scer\GAL4da.PU rescues the wing posture defect and thoracic muscle apoptosis phenotype of Pink1B9/Pink1B9 mutants. Expression of dj-1βScer\UAS.cMa under the control of Scer\GAL4da.PU partially rescues the wing posture defect of Pink1B9/Pink1B9 mutants. Expression of DJ-1αScer\UAS.cUa under the control of Scer\GAL4da.PU rescues the thoracic muscle defects and thoracic muscle apoptosis phenotype, and partially rescues the wing posture defect of Pink1B9/Pink1B9 mutants. Expression of dj-1βC45A.Scer\UAS under the control of Scer\GAL4da.PU rescues the thoracic muscle apoptosis phenotype, and partially rescues the wing posture defect of Pink1B9/Pink1B9 mutants.
The defects in the adult thorax, the progressive abnormal wing posture phenotype, the progressive loss of climbing ability and the shorter lifespan seen in Pink1B9 flies are suppressed if they are also mutant for either Pgam5NP0568 or Pgam51. The progressive abnormal wing posture phenotype, the progressive loss of climbing ability and the reduction in lifespan seen in Pink1B9 flies are enhanced by expression of Pgam5Scer\UAS.cIa under the control of Scer\GAL4da.G32. The mitochondrial hyperfusion and loss of cristae of the mitochondria of indirect flight muscles of one day old Pink1B9 adults is partially suppressed by either Pgam5NP0568 or Pgam51. 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 Pink1B9 adults is suppressed if the flies are also mutant for Pgam5NP0568 or Pgam51.
The downturned wing, crushed thorax and flightless phenotypes of Pink1B9 mutant flies are suppressed by expression of Drp1Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4hs.PB. The downturned wing and crushed thorax phenotypes of Pink1B9 mutant flies are enhanced by expression of Drp1K38A.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4hs.PB. The downturned wing, crushed thorax and flightless phenotypes of Pink1B9 mutant flies are not suppressed by Drp12/+. The downturned wing, crushed thorax and flightless phenotypes of Pink1B9 mutant flies are not suppressed by expression of opa1-likeScer\UAS.T:Zzzz\FLAG under the control of Scer\GAL4hs.PB. The downturned wing and crushed thorax phenotypes but not the flightless phenotype of Pink1B9 mutant flies is significantly suppressed by opa1-likeEY09863/+. Expression of MarfGD11094 under the control of Scer\GAL4hs.PB strongly suppresses the downturned wing and crushed thorax phenotypes of Pink1B9 mutant flies and the flightless phenotype is partially suppressed. The downturned wing, crushed thorax and flightless phenotypes of Pink1B9 mutant flies are not suppressed by expression of MarfScer\UAS.T:Zzzz\FLAG under the control of Scer\GAL4hs.PB. The swollen mitochondria phenotype seen in dopaminergic neurons of Pink1B9 mutants is suppressed by expression of one of parkScer\UAS.T:Hsap\MYC or Drp1Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4ple.PF. The swollen mitochondria phenotype seen in dopaminergic neurons of Pink1B9 mutants is not suppressed by Drp12/+ but is significantly rescued by opa1-likeEY09863/+.
The climbing ability of park25 Pink1B9 double mutants is not significantly different from the climbing ability of either single mutant. The climbing ability of HtrA2Δ1 Pink1B9 double mutants is not significantly different from the climbing ability of the Pink1B9 single mutant. The defects in climbing ability that are seen in Pink1B9 mutants are suppressed by expression of HtrA2Scer\UAS.P\T.cTa under the control of Scer\GAL4Act.
Thor2/Thor2; Pink1B9/Pink1B9 double mutants show partial lethality (unlike either viable single mutant or viable single mutants with the other allele heterozygotic), with rare escapers dying soon after eclosion; expression of ThorScer\UAS.cMa driven by Scer\GAL4da.PU suppresses this lethality in double mutants. Expression of ThorScer\UAS.cMa driven by Scer\GAL4how-24B significantly partially suppresses flight and climbing defects as well as muscle degeneration and mitochondrial disruption in Pink1B9/Pink1B9 flies. Expression of ThorScer\UAS.cMa driven by Scer\GAL4ple.PF significantly suppresses loss of dopaminergic PPL1 neurons in 30 day old Pink1B9/Pink1B9 flies. Expression of foxoScer\UAS.cFa in a Pink1B9/Pink1B9 background results in lethality. Lrrke03680 suppresses flight and climbing defects as well as dopaminergic PPL1 neuron loss in Pink1B9/Pink1B9 flies.
Expression of parkScer\UAS.T:Zzzz\FLAG,T:Hsap\COX4I1 under the control of Scer\GAL4hs.PB suppresses the mitochondrial swelling phenotype in Pink1B9, park1 double mutants to a great extent. Expression of parkScer\UAS.T:Hsap\MYC under the control of Scer\GAL4hs.PB partially suppresses the mitochondrial swelling phenotype in Pink1B9, park1 double mutants. Expression of parkT187A.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4hs.PB partially suppresses the mitochondrial swelling phenotype in Pink1B9, park1 double mutants.
Expression of parkScer\UAS.cGa under the control of Scer\GAL4Mef2.PR fully rescues the thoracic indentation and flight phenotypes of Pink1B9 mutants. Drp1T26/+ or Drp1KG03815/+ in combination with Pink1B9 hemizygous mutations results in almost complete lethality. The few surviving adults are developmentally delayed and are substantially smaller and short lived than single Pink1B9 hemizygous mutants. Viability of Drp1T26/+ or Drp1KG03815/+ flies is unaffected in a heterozygous Pink1B9/+ background. Expression of Drp1T:Zzzz\FLAG,T:Zzzz\TC,T:Ivir\HA1 or Drp1+t9.4 results in partial rescue of the thoracic indentation and impaired flight phenotypes of Pink1B9 hemizygous mutants, and expression of Drp1+t9.4 partially rescues the impaired climbing phenotype and mitochondrial morphological defects of Pink1B9 hemizygous mutants. Opa1s3475/+ partially suppresses the thoracic indentation, impaired flight, impaired climbing, and mitochondrial morphology phenotypes of Pink1B9 hemizygous mutants. Opa1f02779/+ partially suppresses the thoracic indentation and impaired flight phenotypes of Pink1B9 hemizygous mutants.
Pink1B9 does not suppress the eye pigmentation loss seen in flies expressing HtrA2Scer\UAS.cPa under the control of Scer\GAL4GMR.PF. Pink1B9 partially suppresses the rough eye phenotype seen when rho-7Scer\UAS.cWa is expressed under the control of Scer\GAL4GMR.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 Pink1B9 flies is suppressed by Drp1T:Zzzz\FLAG,T:Zzzz\TC,T:Ivir\HA1 or by opa1-likeEY09863/+. The mitochondrial aggregation phenotype seen in the dorsolateral protocerebral posterior DA (dopaminergic) neuron cluster in Pink1B9 animals is suppressed by Drp1T:Zzzz\FLAG,T:Zzzz\TC,T:Ivir\HA1 or by opa1-likeEY09863/+. The mitochondrial aggregation phenotype seen in the dorsolateral protocerebral posterior DA (dopaminergic) neuron cluster in Pink1B9 animals is suppressed by expression of parkScer\UAS.T:Ivir\HA1 under the control of Scer\GAL4ple.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.
Xenogenetic Interactions
Statement
Reference
The increased relative mitochondrial content exhibited during pupariation by enterocytes in Pink1B9 homozygous midgut clones is suppressed by the clonal expression of Hsap\PARK2Scer\UAS.cYa under the control of Scer\GAL4Act.PU.
Expression of Hsap\BNIP3LScer\UAS.cGa under the control of Scer\GAL4hs.PU rescues the fragmented mitochondrial morphology of Pink1B9/Pink1B9 mutants.
Heterozygous Pink1B9 does not decrease life span in flies expressing Scer\GAL4elav.PU>Hsap\HTTQ93.ex1p.Scer\UAS.
Expression of Hsap\VPS35Scer\UAS.cMa under the control of Scer\GAL4da.PU does not suppress the climbing defects seen in Pink1B9 mutant flies. The flight defects seen in Pink1B9 mutants are enhanced.
Thoracic indentations seen in Pink1B9/y males are partially suppressed by expression of Hsap\CLUHScer\UAS.P\T.cSa driven by Scer\GAL4Mhc.PW.
Ubiquitous expression of Scer\NDI1Scer\UAS.cVa under the control of Scer\GAL4da.PU partially rescues the climbing defects seen in Pink1B9 mutant flies. The flight defects are not significantly rescued.
Expression of Scer\GAL4da.G32>Hsap\FBXO7Scer\UAS.cBb is not able to rescue the Pink1B9 locomotor deficits, neuron loss, muscle degeneration or mitochondrial disruption.
Expression of Hsap\TRAP1Scer\UAS.cBa under the control of Scer\GAL4da.G32 partially rescues the abnormal wing posture and thorax indentations seen in Pink1B9/Y flies. The reduced climbing index seen in Pink1B9/Y flies is suppressed, while the reduction in flight ability is not suppressed in the rescued flies. Expression of Hsap\TRAP1Scer\UAS.cBa under the control of Scer\GAL4da.G32 rescues the vacuolisation and abnormal mitochondrial morphology seen in the indirect flight muscles of Pink1B9/Y flies. Expression of Hsap\TRAP1D158N.Scer\UAS under the control of Scer\GAL4da.G32 does not rescue the abnormal wing posture, thorax indentations, reduced climbing ability or reduction in flight ability seen in Pink1B9/Y flies. Expression of Hsap\TRAP1D158N.Scer\UAS under the control of Scer\GAL4da.G32 fails to rescue the vacuolisation and abnormal mitochondrial morphology seen in the indirect flight muscles of Pink1B9/Y flies.
Scer\NDI1Scer\UAS.cVa (in the absence of a Scer\GAL4 driver) rescues the sterility of Pink1B9 male flies. Expression of Scer\NDI1Scer\UAS.cVa under the control of Scer\GAL4da.G32 partially suppresses the flight defects of Pink1B9 flies. The defects in organisation of the mitochondria which are seen in the indirect flight muscles of Pink1B9 flies are also partially suppressed by expression of Scer\NDI1Scer\UAS.cVa under the control of Scer\GAL4da.G32. Expression of Zzzz\AOXScer\UAS.cFa under the control of Scer\GAL4da.G32 does not suppress the male sterility, flight defects or defects in mitochondrial morphology seen in Pink1B9 flies.
Expression of either Tcas\PINK1Scer\UAS.cWa or Phum\PINK1Scer\UAS.cWa under the control of Scer\GAL4da.G32 rescues the defects in climbing and flight ability and the appearance of thoracic indentations in Pink1B9 flies.
Expression of Hsap\PARK7Scer\UAS.cMa under the control of Scer\GAL4da.PU partially rescues the wing posture defect of Pink1B9/Pink1B9 mutants.
Expression of Hsap\PINK1Scer\UAS.T:Zzzz\FLAG under the control of Scer\GAL4elav.PU rescues the defects in mobilisation of the reserve pool of synaptic vesicles which are seen in Pink1B9 mutant larvae. Expression of Hsap\PINK1G309D.Scer\UAS.T:Zzzz\FLAG under the control of Scer\GAL4elav.PU does not rescue the defects in mobilisation of the reserve pool of synaptic vesicles which are seen in Pink1B9 mutant larvae.
Complementation and Rescue Data
Comments
The reduced climbing ability, abnormal swollen mitochondria, disorganized muscle fibres as well as the decreased number of brain dopaminergic neurons characteristic for Pink1B9 adults is rescued by combination with any of the following: Pink1S346D.KD.GMR.T:Mito-Tom20,T:Avic\GFP, Pink1S519A.GMR.T:Mito-Tom20,T:Avic\GFP or Pink1GMR.T:Mito-Tom20,T:Avic\GFP (but not Pink1S346A.GMR.T:Mito-Tom20,T:Avic\GFP).
The enlarged or aggregated mitochondria phenotype observed in the body wall muscles of Pink1B9 hemizygous male third instar larvae is restored by expression of Pink1Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4how-24B.
Expression of Pink1Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4elav.PU rescues the loss of dopaminergic neurons in the PPL1 cluster and adult thorax defects of Pink1B9 flies.
Expressing Pink1Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4hs.PB rescues the crushed thorax and downturned wing phenotypes seen in Pink1B9 mutant flies at both 3 and 45 days post-eclosion. The mitochondrial defects, reduction in ATP levels and flightlessness are also rescued. Expression of Pink1Scer\UAS.T:Ivir\HA1 suppresses the dopaminergic neuron loss in 45 day old Pink1B9 mutant flies. Expressing Pink1K337R.D479A.D501A.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4hs.PB fails to rescue the crushed thorax and downturned wing phenotypes seen Pink1B9 mutant flies at 3 days post-eclosion. The mitochondrial defects, reduction in ATP levels and flightlessness are also not rescued. Expression of Pink1K337R.D479A.D501A.Scer\UAS.T:Ivir\HA1 fails to rescue phenotypes seen in 45 day old Pink1B9 mutant flies, with both the downturned wing and dopaminergic neuron loss still seen in these flies. Expressing Pink1G426D.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4hs.PB rescues the crushed thorax and downturned wing phenotypes seen in Pink1B9 mutant flies at three days post-eclosion. The mitochondrial defects, reduction in ATP levels and flightlessness are also suppressed. However expression of Pink1G426D.Scer\UAS.T:Ivir\HA1 fails to rescue the phenotypes seen in 45 day old Pink1B9 mutant flies; as in Pink1B9 alone, the flies have downturned wings, the thoracic muscles contain abnormally swollen mitochondria between sparse muscle fibres, ATP levels are reduced and the flies are unable to fly. The loss of dopaminergic neurons seen in Pink1B9 is also still present. Expressing Pink1L464P.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4hs.PB fails to rescue the crushed thorax and downturned wing phenotypes seen in Pink1B9 mutant flies at three day post-eclosion. The mitochondrial defects, reduction in ATP levels and flightlessness are also still present. Expression of Pink1L464P.Scer\UAS.T:Ivir\HA1 fails to rescue the dopaminergic neuron loss seen in 45 day old Pink1B9 mutant flies.
Expression of Pink1Scer\UAS.cUa under the control of Scer\GAL4da.PU partially rescues the wing posture defect of Pink1B9/Pink1B9 mutants.
Expression of Pink1K337R.D479A.D501A.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4hs.PB fails to rescue the apparent behavioural phenotypes of Pink1B9 mutants. Impaired mitochondria in the indirect flight muscle of Pink1B9 mutants are not recovered by Pink1K337R.D479A.D501A.Scer\UAS.T:Ivir\HA1 expression under the control of Scer\GAL4hs.PB. Expression of Pink1Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4hs.PB almost fully rescues the apparent behavioural phenotypes of Pink1B9 mutants. Similarly, impaired mitochondria in the indirect flight muscle of Pink1B9 mutants are fully recovered by Pink1Scer\UAS.T:Ivir\HA1 expression under the control of Scer\GAL4hs.PB.
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