dPINK1, Pink
promotes mitochondrial fragmentation by targeting core components of the mitochondrial morphogenesis machinery for ubiquitination - negatively regulates mitochondrial fusion - a fruitfly model for Parkinson's disease
Please see the JBrowse view of Dmel\Pink1 for information on other features
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AlphaFold produces a per-residue confidence score (pLDDT) between 0 and 100. Some regions with low pLDDT may be unstructured in isolation.
Gene model reviewed during 5.52
Low-frequency RNA-Seq exon junction(s) not annotated.
Annotated transcripts do not represent all supported alternative splices within 5' UTR.
Annotated transcripts do not represent all possible combinations of alternative exons and/or alternative promoters.
Gene model reviewed during 5.55
Interacts with park (PubMed:19048081). Interacts with rho-7 and HtrA2 (PubMed:19048081).
Proteolytically cleaved (PubMed:19048081). In healthy cells, the precursor is continuously imported into mitochondria where it is proteolytically cleaved into its short form by the mitochondrial rhomboid protease rho-7 (PubMed:19048081). The short form is then released into the cytosol where it rapidly undergoes proteasome-dependent degradation (Probable). In unhealthy cells, when cellular stress conditions lead to the loss of mitochondrial membrane potential, mitochondrial import is impaired leading to the precursor accumulating on the outer mitochondrial membrane (OMM) (PubMed:27906179).
Autophosphorylated on Ser-346, which activates kinase activity (PubMed:25474007, PubMed:27906179). Loss of mitochondrial membrane potential results in the precursor accumulating on the outer mitochondrial membrane (OMM) where it is activated by autophosphorylation at Ser-346 (PubMed:27906179). Autophosphorylation is sufficient and essential for selective recruitment of park to depolarized mitochondria, likely via Pink1-dependent phosphorylation of polyubiquitin chains (PubMed:25474007, PubMed:27906179).
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\Pink1 using the Feature Mapper tool.
Comment: maternally deposited
GBrowse - Visual display of RNA-Seq signals
View Dmel\Pink1 in GBrowse 21-18
1-18.6
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 identity of: Pink1 CG4523
Source for merge of: CG4523 BEST:GH23468
Mutants are viable but sterile. Mutant spermatids form abnormal Nebenkerns and mitochondrial derivatives and subsequently fail to individualize the 64-cell cyst into discrete sperm. Mutants show increased sensitivity to paraquat and hyperoxia and have heldup wings due to degeneration of indirect flight muscle.
Pink1 is required for normal mitochondrial function.
Mutants show a number of degenerative phenotypes which are due to mitochondrial dysfunction.
Pink1 plays an important role in regulating energy metabolism and exerts an impact on lifespan.
Pink1 plays a critical role in promoting dopaminergic neuronal function and survival.
Pink1 mutants exhibit age-dependent muscle degeneration characterised by extensive DNA fragmentation, probably indicative of cell death.
Pink1 is required for maintaining proper mitochondria morphology and the integrity of suets of muscle cells and dopaminergic neurons.
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.