dParkin, D-parkin, dpk
ubiquitin protein ligase - degrades proteins with aberrant conformations - mutants exhibit muscle degeneration, male sterility, and defects in brain dopaminergic cells - PINK1 activates Parkin activity leading to ubiquitination of multiple proteins, which in turn promotes clearance of mitochondria by mitophagy
Please see the JBrowse view of Dmel\park for information on other features
To submit a correction to a gene model please use the Contact FlyBase form
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.45
50-55 (kD)
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\park using the Feature Mapper tool.
Comment: rapidly degraded
park transcript is expressed in 0-2 hr embryos, and in third instar larvae through adults.
In the germarium, park protein is specifially detected in germarium region 2b. In egg chambers park protein is detected up to stage 9-10 in the oocyte. It is preferentially localized at the posterior pole and is specifically expressed in the anterior margin of the oocyte. It colocalizes with eIF4E1 protein in the oocyte.
GBrowse - Visual display of RNA-Seq signals
View Dmel\park in GBrowse 23-47
maps to 3L
Please Note FlyBase no longer curates genomic clone accessions so this list may not be complete
Please Note This section lists cDNAs and ESTs that fall within the genomic extent of the gene model, which may include cDNAs and ESTs of genes within introns, or of overlapping genes. Please see GBrowse for alignment of the cDNAs and ESTs to the gene model.
For each fully sequenced cDNA the DGRC maintains various forms of the cDNA (e.g tagged or untagged) in several different host vectors for subsequent cloning and expression in Drosophila and Drosophila cell lines.
polyclonal
Source for merge of: parkin CG10523
Source for merge of parkin CG10523 was sequence comparison ( date:020502 ).
park is required for the regulation of tubulin levels.
The condition of park mutants raised on zinc-supplemented food is greatly improved.
Flies mutant for park show significantly reduced lifespan but no difference in dopamine neuron numbers when raised on food supplemented with environmental pesticides or mitochondrial toxins.
The increased lifespan of park mutants is due to metal chelation.
park mutants display increased vulnerability to environmental pesticides and mitochondrial toxins associated with Parkinson's disease.
park gene function is necessary for mitochondrial morphogenesis during earlier and later phases of spermiogenesis.
In park mutants, the investment cones are scattered along the post-elongated spermatid bundles and fail to act properly in the process of sperm individualization.
The level of dopamine is significantly reduced in park mutants compared to controls.
Inhibition of park leads to a reduction of phospho-Akt levels.
park appears to have a role in mitochondrial function.