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General Information
Symbol
Dmel\parkΔ21
Species
D. melanogaster
Name
FlyBase ID
FBal0158835
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
parkinΔ21
Key Links
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

Deletion of sequence between insertion sites of P{EP}parkP21 and P{EP}parkP30.

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 ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In

indirect flight muscle & mitochondrion

indirect flight muscle & nuclear membrane

Detailed Description
Statement
Reference

parkΔ21/park1 mutants exhibit muscle cell abnormalities and degeneration (accumulation of ubiquitin modified proteins and disordering of actin filaments) with large and dysmorphic mitochondria (Mito-GFP) when compared to controls. Also these mutants are incapable of flight.

Body wall muscles in parkΔ21/parkf01950 transheterozygous and parkΔ21/park13 transheterozygous third instar larvae frequently show nuclei clustering together or in contact with each other, instead of the typically even spaced in controls; parkΔ21/park13 transheterozygous muscles exhibit larger and more globular mitochondria; parkΔ21/parkf01950 nuclei also exhibit a smaller size and an irregular shape (uneven nuclear envelope). Nuclei clustering is not observed in the parkΔ21 heterozygous background.

park1/parkΔ21 transheterozygous adults display aberrant wing posture, thoracic indentations and climbing ability deficit along with mitochondrial defects (loss of cristae) in indirect flight muscles.

parkΔ21/park1 transheterozygotes present mitochondria fragmentation, despite of normal cristae morphology, in adult indirect flight muscles, as compared to controls.

These heterozygote adults are short lived compared to controls.

The indirect flight muscles of flies expressing parkSA.Scer\UAS under the control of Scer\GAL4da.PU in a parkΔ21/park1 mutant background contain abnormally fused mitochondria.

The flight muscles of park1/parkΔ21 adults have swollen mitochondria.

park1/parkΔ21 flies often have an abnormal wing posture, and mitochondrial aggregation is seen in the muscles.

The flight defects of park1/parkΔ21 animals are significantly improved by feeding with vitamin K[[2]] (MK-4 form tested).

The mitochondrial morphology defects of park1/parkΔ21 larvae are partially rescued by feeding with vitamin K[[2]] (MK-4 form tested).

parkΔ21 homozygotes are adult viable but eclose one day later than heterozygous controls, but show significant pupal lethality (68% of park mutant pupae fail to eclose. parkΔ21 homozygous adults are significantly smaller and around 30% lighter than controls of the same age and sex. Compared with heterozygous controls, cell size in the wings of parkΔ21 homozygous females is reduced by 10% and the wing area itself is reduced by 23%. The mean life spans for parkΔ21 homozygote and for parkΔ21/Df(3L)Pc-MK flies are 13 and 32 days respectively, compared to a mean life span of >60 days in heterozygous controls. The files are also more sensitive to cold and to paraquat (2mM) than heterozygous controls. parkΔ21 homozygotes show a much reduced jump response than heterozygous controls and are flightless with drooped wings. Analysis of indirect flight muscles in these flies reveals degeneration which increases with age. Ultrastructural analysis of these muscles at 2 days post eclosion reveals increased spacing between fibril groups, a reduced number of fibrils, reduced numbers of mitochondria (which are of a generally smaller with a significant loss of christae), chromatin condensation and nuclear envelope breakdown. parkΔ21 homozygotes do not show any loss of dopaminergic neurons in the dorsal-medial clusters of the brain, in 2-3 day or 21 day old animals, and have normal electroretinograms at 2 weeks of age.

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

parkΔ21/park1 has abnormal flight phenotype, non-suppressible by mAcon11/Acon[+]

parkΔ21/park1 has abnormal flight phenotype, non-suppressible by mAcon1MB09176/Acon[+]

parkΔ21/park1 has male sterile phenotype, non-suppressible by Scer\NDI1UAS.cVa

parkΔ21 has sterile phenotype, non-suppressible by Pink1βTub85D.PC

Enhancer of
Suppressor of
Statement
Reference
Other
Phenotype Manifest In
NOT Enhanced by
Statement
Reference
Suppressed by
Statement
Reference

parkΔ21/park25 has adult external thorax phenotype, suppressible | partially by mask[+]/mask10.22

NOT suppressed by
Statement
Reference
Enhancer of
Statement
Reference
Suppressor of
Other
Additional Comments
Genetic Interactions
Statement
Reference

Body wall muscles in ari-1A/+,parkΔ21/+ or ari-1A/Y,parkΔ21/+ third instar larvae frequently show nuclei clustering together or in contact with each other, instead of the typically even spaced in controls; these nuclei also exhibit a smaller size and an irregular shape (uneven nuclear envelope).

The mitochondria morphology defects observed in the adult indirect flight muscles of parkΔ21/park1 transheterozygotes are not enhanced by Chchd2H43 homozygosity.

Expression of maskHMS01045 RNAi suppresses the short lived phenotype of park25/parkΔ21 transheterozygote adults.

The mitochondria morphological defects seen in park1/parkΔ21 adults are not rescued by Acon1/+ or AconMB09176/+.

Expression of either rictorScer\UAS.cHa or trcS292E.Scer\UAS under the control of Scer\GAL4da.PU fails to rescue the abnormal wing posture and mitochondrial aggregation phenotypes seen in park1/parkΔ21 flies.

Heterozygosity for parkΔ21 enhances the loss of dopaminergic neurons in the dorsomedial clusters of 40-day old adult brains caused by expression of Sep4Scer\UAS.cMa under the control of Scer\GAL4Ddc.PL.

Heterozygosity for parkΔ21 increases the percentage of Sep4Scer\UAS.cMa, Scer\GAL4da.G32 flies showing a wrinkled wing phenotype.

The mild rough eye phenotype seen in flies expressing Sep4Scer\UAS.cMa under the control of Scer\GAL4GMR.PF is enhanced in flies heterozygous for either parkΔ21 or Df(3L)Pc-MK, and is further enhanced in parkΔ21/Df(3L)Pc-MK trans-heterozygous flies.

Xenogenetic Interactions
Statement
Reference

Scer\NDI1Scer\UAS.cVa in the absence of a Scer\GAL4 driver does not suppress the sterility of park1/parkΔ21 males (even though Scer\NDI1Scer\UAS.cVa in the absence of a Scer\GAL4 driver does suppress the male sterility of Pink1B9 males).

Expression of Scer\NDI1Scer\UAS.cVa under the control of Scer\GAL4da.G32 does not suppress the flight defects or defects in mitochondrial morphology which are seen in park1/parkΔ21 flies.

Complementation and Rescue Data
Partially rescued by
Comments

Expression of parkScer\UAS.cGa under the control of the Scer\GAL4how-24B driver rescues the defective mitochondria observed in body wall muscles of park25/parkΔ21 third instar larvae.

Expression of parkScer\UAS.cSa under the control of Scer\GAL4da.PU rescues the mitochondria phenotype seen in parkΔ21/park1 mutant indirect flight muscles. The reduction in ATP levels is also rescued, and is improved to a level higher than that of controls.

Expression of parkScer\UAS.cSa under the control of Scer\GAL4Mhc.PU rescues the wing posture and thorax defects seen in parkΔ21/park1 mutant flies.

Expression of parkSA.Scer\UAS under the control of Scer\GAL4da.PU fails to rescue the mitochondria phenotype seen in parkΔ21/park1 mutant indirect flight muscles. The reduction in ATP levels is rescued, and is improved to a level higher than that of controls.

Expression of parkSA.Scer\UAS under the control of Scer\GAL4Mhc.PU partially rescues the wing posture and thorax defects seen in parkΔ21/park1 mutant flies. The reduction in ATP levels is also improved.

Expression of parkSE.Scer\UAS under the control of Scer\GAL4da.PU results in lethality, either in a parkΔ21/park1 or wild type mutant background.

The reduced body size/mass, reduced lifespan and increased sensitivity to cold an paraquat seen in parkΔ21 homozygous adults are all partially rescued by park+tR, but not by parktSR. Reduced jump response, flightlessness and indirect flight muscle degeneration in parkΔ21 homozygotes are completely rescued by park+tR, but not by parktSR. Flightlessness is also rescued by expression of parkScer\UAS.T:Ivir\HA1 with Scer\GAL4c179 or Scer\GAL4Ubi.

Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (7)
References (21)