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General Information
Symbol
Dmel\ParpCH1
Species
D. melanogaster
Name
FlyBase ID
FBal0138435
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
CH(3)1
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

P{PZ} insertion near the upstream promoter of the Parp e isoform.

Insertion components
P{PZ}ParpCH1
Product class / Tool use(s)
Encoded product / tool
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 ( 0 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 1 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

ParpCH1 heterozygous mutant adults do not present altered oxygen consumption and do not present brain mitochondria with altered potential, as compared to controls.

ParpCH1/+ mutants display no reduction in dopaminergic PPL1 neuron number as compared to controls.

ParpCH1 cells lack nucleoli. Only 10% of ParpCH1 third instar larvae survive a 40-min heat shock, while 99% of wild-type larvae survive.

The average size of the heat shock puffs at 87A and 87C on the polytene chromosomes is reduced threefold in mutant larvae compared to wild type. Mutant larvae often develop intracellular bacterial infections, which is rarely seen in wild type. The larvae are also sensitive to experimental infection; 95% die after a dose of injected E.coli that kills less than 7% of controls.

Homozygotes develop slowly and usually die during the second instar stage after 6-9 days. The brain is of normal size. Up to 50% of the larvae are arrested at the onset of ecdysis II (as seen by the phenotype of the mouth hooks). Nuclear morphology is dramatically altered in mutants; the nuclei appear more uniform than wild type, have a less distinct chromocenter and lack a nucleolar region of low DNA density.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressor of
Statement
Reference

Parp[+]/ParpCH1 is a suppressor of decreased cell number | adult stage phenotype of Pink1B9

Parp[+]/ParpCH1 is a suppressor | partially of short lived phenotype of Pink1B9

Parp[+]/ParpCH1 is a suppressor of abnormal neuroanatomy | adult stage phenotype of Pink1B9

Parp[+]/ParpCH1 is a suppressor | partially of short lived phenotype of park25

Parp[+]/ParpCH1 is a suppressor | partially of visible phenotype of park25

Parp[+]/ParpCH1 is a suppressor of abnormal neuroanatomy | adult stage phenotype of park25

Phenotype Manifest In
Suppressor of
Statement
Reference

Parp[+]/ParpCH1 is a suppressor | partially of adult thorax phenotype of Pink1B9

Parp[+]/ParpCH1 is a suppressor | partially of adult brain phenotype of Pink1B9

Parp[+]/ParpCH1 is a suppressor | partially of neuropil | adult stage phenotype of Pink1B9

Parp[+]/ParpCH1 is a suppressor | partially of mitochondrial crista | adult stage phenotype of Pink1B9

Parp[+]/ParpCH1 is a suppressor of dopaminergic PPL1 neuron | adult stage phenotype of Pink1B9

Parp[+]/ParpCH1 is a suppressor | partially of adult thorax phenotype of park25

Parp[+]/ParpCH1 is a suppressor of dopaminergic PPL1 neuron phenotype of park25

Additional Comments
Genetic Interactions
Statement
Reference

ParpCH1 heterozygosity leads to a significant suppression of the defects in lifespan, climbing capacity, thorax morphology, number of dopaminergic PPL1 neurons, mitochondria cristae morphology in the neuropil and oxygen consumption, observed in Pink1B9 homozygous mutant adults; ParpCH1 also rescues the decreased mitochodria potential observed in the brains of Pink1B9 homozygous mutant adults.

park25, ParpCH1/+ double mutants display a reduced thoracic defect, and partially rescued climbing performance and survival, as compared to park25 mutants. The dopaminergic neuron phenotype of park25 is fully rescued in park25, ParpCH1/+ double mutants.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Fails to complement
Partially rescued by
Comments
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
Comments
Comments

Excision of the P{PZ} element can revert the lethal phenotype.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (8)