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General Information
Symbol
Dmel\Pink15
Species
D. melanogaster
Name
FlyBase ID
FBal0196293
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Imprecise excision of the insertion in Pink1G900, resulting in a deletion of Pink1 sequences, including the mitochondrial targeting sequence and over 70% of the kinase domain.

Expression Data
Reporter Expression
Additional Information
Statement
Reference
 
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 1 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 1 )
Disease
Interaction
References
is ameliorated by Mul1UAS.cYa
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In

mitochondrial crista & indirect flight muscle

Detailed Description
Statement
Reference

The DA neurons of Pink15 adults exhibit aggregated or elongated mitochondria.

Pink15/+ heterozygous mutants have significantly reduced mitochondrial length and significantly increased mitochondrial number in axons of adult neurons, compared to controls.

Pink15 mutant embryos display asymmetric frontal ganglia and altered esophageal ganglia, as compared to controls.

Pink15 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, a "vacuole" phenotype and decreased number of crista junctions, but no changes in mitochondria size; there are no obvious muscle degeneration signs in these larvae. In the nervous system, mitochondria cristae defects are observed in the ventral nerve cord neuropils (synapses, dendrites, and axons, but not in the cell bodies), in the segmental nerves (axons), and at the neuromuscular junctions. These larvae have impaired crawling ability.

In 3 days old Pink15 hemizygous male adults, indirect flight muscles present vacuolated and "onion"-like mitochondria, all of which convert to vacuolated mitochondria at day 5; at day 5 these indirect flight muscles show signs of degeneration.

Pink15 mutant escapers do not exhibit lipid droplet accumulation. Aconitase activity is reduced in these mutants and there is a strong correlation between decreased aconitase enzymatic activity and the number of lipid droplets per ommatidium, suggesting reactive oxygen species may play a role in lipid droplet accumulation.

Pink15 mutant flies show elevated response across a range of spatiotemporal frequencies of contrast-reversing sine-wave gratings as compared to responses from control flies.

PPL1 dopaminergic neurons in the brain have abnormally clumped mitochondria in mutant adults.

Mutants show severe defects in mitochondrial morphology in the indirect flight muscle (IFM): mitochondrial size is irregular and clumping of mitochondria are seen. Many of the mitochondria are swollen and have fragmented cristae. The mutant muscle shows cell death and vacuolisation, indicating degeneration. The mutant adults have a thoracic indentation due to this degeneration of the IFM.

Mutant spermatids show vacuolated onion-stage nebenkerns, and in subsequent stages, show only one mitochondrial derivative rather than the normal two seen in wild-type spermatids. A cross-section through mutant sperm tails shows the presence of only the major mitochondrial derivative, but not the minor mitochondrial derivative.

Indirect flight muscles of mutant flies show severe defects in mitochondrial morphology, including swollen mitochondria with broken cristae. Vacuolisation, indicative of degeneration, is seen in the indirect flight muscles.

Mutant adults have an abnormal wing posture.

Pink15 mutant males exhibit mitochondrial morphology defects in the testes. Spermatids show vacuolisation in the spherical "onion stage" nebenkern. Only one mitochondrial derivative is seen during spermatid elongation (the "leaf blade" stage), as opposed to the two usually seen in wild type. Pink15 mutant spermatids also exhibit dramatic defects in mitochondrial morphology during the post-individualisation stages.

An-age dependent decrease in the number of dopaminergic neurons is seen in Pink15 mutant flies. Fewer neurons are observed in 40 day old flies at 25[o]C. Pink15 mutant flies also show striking indirect flight muscle degeneration and severely disrupted mitochondrial morphology with broken cristae.

Indirect flight muscles of 1-2 day old mutant adults show a marked increase in TUNEL-positive nuclei compared to controls, indicating an increase in the number of apoptotic cells.

Mutant flies show a 59% reduction in resistance to paraquat and a 71% reduction in resistance to rotenone compared to controls. They are also more sensitive to dithiothreitol and to high concentrations of salt compared to wild-type flies.

Mutant males show vacuolation of Nebenkern in the testes.

The indirect flight muscles of 2 day old flies have mitochondria with fragmented cristae.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
NOT suppressed by
Statement
Reference
Suppressor of
Statement
Reference
NOT Suppressor of
Statement
Reference

Pink15/Pink15 is a non-suppressor of visible | heat sensitive phenotype of HtrA2UAS.cYa, Scer\GAL4GMR.PF

Phenotype Manifest In
Enhanced by
Statement
Reference

Pink15 has adult thorax | dorsal phenotype, enhanceable by Mul1A6

NOT Enhanced by
Statement
Reference

Pink15 has adult thorax | dorsal phenotype, non-enhanceable by park25

Pink15 has spermatid phenotype, non-enhanceable by HtrA2NSO/Df(3R)ED5644

Pink15 has Nebenkern phenotype, non-enhanceable by HtrA2NSO/Df(3R)ED5644

Suppressed by
Statement
Reference

Pink15 has axon | adult stage phenotype, suppressible | clone of cells by gfzf541

Pink15 has wing phenotype, suppressible by Drp1UAS.cDa/Scer\GAL4Mef2.PR

Pink15 has Nebenkern phenotype, suppressible | partially by parkβTub85D.PC

Pink15 has mitochondrial crista & indirect flight muscle phenotype, suppressible | partially by Scer\GAL4how-24B/Scer\GAL4how-24B/parkUAS.cGa

NOT suppressed by
Statement
Reference

Pink15 has spermatid phenotype, non-suppressible by HtrA2βTub85D.PY

Pink15 has Nebenkern phenotype, non-suppressible by HtrA2βTub85D.PY

NOT Enhancer of
Statement
Reference

Pink15 is a non-enhancer of adult thorax | dorsal phenotype of park25

Suppressor of
Statement
Reference
NOT Suppressor of
Statement
Reference

Pink15/Pink15 is a non-suppressor of eye | heat sensitive phenotype of HtrA2UAS.cYa, Scer\GAL4GMR.PF

Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

Expression of Mul1Scer\UAS.cYa under the control of Scer\GAL4ple.PF suppresses the abnormal clumping of mitochondria seen in the PPL1 dopaminergic neurons of Pink15 adults.

Expression of Mul1Scer\UAS.cYa under the control of Scer\GAL4Mef2.PU suppresses almost all the defects seen in the indirect flight muscles of Pink15 adults and the thoracic indentation phenotype is also suppressed.

Expression of Mul1LD.Scer\UAS under the control of Scer\GAL4Mef2.PU does not suppress the abnormal clumping of mitochondria or muscle cell death seen in the indirect flight muscles of Pink15 adults. The thoracic indentation seen in Pink15 adults is also not suppressed.

The degree of thoracic indentation seen in park25 Pink15 double mutants is the same as that seen in either single mutant. The mitochondrial morphology in the indirect flight muscles of the double mutants is similar to that seen in the single mutants.

The degree of thoracic indentation seen in Pink15 Mul1A6 is much more severe than that seen in Pink15 single mutants.

The indirect flight muscles of Pink15 Mul1A6 mutants have highly elongated and interconnected mitochondria.

Pink15/Y ; fzo1/Df(3R)P2O double mutants have nebenkern and mitochondrial derivative phenotypes similar to those of Pink15/Y single mutants.

Expression of parkScer\UAS.cGa under the control of Scer\GAL4Mef2.PR partially rescues the defects in mitochondrial morphology that are seen in the indirect flight muscles of Pink15 mutants.

Expression of either MarfmiRNA.CDS.Scer\UAS or MarfmiRNA.UTR.Scer\UAS under the control of Scer\GAL4Mef2.PR suppresses the defects in mitochondrial morphology that are seen in the indirect flight muscles of Pink15 mutants. The defects in wing posture and indirect flight muscle degeneration phenotypes are also suppressed.

Expression of Drp1Scer\UAS.cDa under the control of Scer\GAL4Mef2.PR suppresses the defects in mitochondrial morphology that are seen in the indirect flight muscles of Pink15 mutants. The defects in wing posture and indirect flight muscle degeneration phenotypes are also suppressed.

Expression of opa1-likemiRNA.CDS.Scer\UAS under the control of Scer\GAL4Mef2.PR suppresses the defects in mitochondrial morphology that are seen in the indirect flight muscles of Pink15 mutants.

Homozygous Pink15 fails to suppress the rough eye phenotype seen when HtrA2Scer\UAS.cYa is expressed under the control of Scer\GAL4GMR.PF at 29[o]C.

Expression of HtrA2βTub85D.PY fails to suppress the mitochondrial morphology defects seen in Pink15 mutant spermatids. The spherical "onion stage" nebenkern contain vacuoles, and only one mitochondrial derivative is seen in "leaf blade stage" elongating spermatids. As in Pink15 mutants alone the flies are sterile.

A HtrA2NSO/Df(3R)ED5644 mutant background does not enhance the mitochondrial morphology defects seen in Pink15 mutant spermatids.

Expression of HtrA2dsRNA.Scer\UAS.cYa under the control of Scer\GAL4Mef2.PR does not enhance the mitochondrial morphology defects seen in Pink15 mutant indirect flight muscles.

The indirect flight muscles of 2 day old Pink15 adults that are also expressing parkScer\UAS.cGa under the control of Scer\GAL4how-24B have some mitochondria with normal densely packed cristae and some with fragmented cristae, in contrast to 2 day old Pink15 single mutants, where the mitochondria of the indirect flight muscles have fragmented cristae.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Not rescued by
Comments

Expression of Pink1Scer\UAS.cCa under the control of Scer\GAL4Mef2.PR completely rescues the defects in mitochondrial morphology that are seen in the indirect flight muscles of Pink15 mutants.

Expression of Pink1βTub85D.PC rescues the mitochondrial morphology defects in Pink15 mutant spermatids. The spherical "onion stage" nebenkern no longer contain vacuoles and, as in wild type, two mitochondrial derivatives are seen in "leaf blade stage" elongating spermatids.

Expression of Pink1Scer\UAS.cCa under the control of Scer\GAL4Mef2.PR rescues the mitochondria morphology defects seen in Pink15 mutant indirect flight muscles.

Expression of Pink1+tCa rescues the male sterility, indirect flight muscle degeneration and mitochondrial defects seen in Pink15 mutant flies.

Expression of Pink1G426D fails to rescue the male sterility, indirect flight muscle degeneration and mitochondrial defects seen in Pink15 mutant flies.

Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
References (14)