JOURNAL ARTICLE

PINK1 is recruited to mitochondria with parkin and associates with LC3 in mitophagy

Sumihiro Kawajiri, Shinji Saiki, Shigeto Sato, Fumiaki Sato, Taku Hatano, Hiroto Eguchi, Nobutaka Hattori
FEBS Letters 2010 March 19, 584 (6): 1073-9
20153330
Mutations in PTEN-induced putative kinase 1 (PINK1) cause recessive form of Parkinson's disease (PD). PINK1 acts upstream of parkin, regulating mitochondrial integrity and functions. Here, we show that PINK1 in combination with parkin results in the perinuclear mitochondrial aggregation followed by their elimination. This elimination is reduced in cells expressing PINK1 mutants with wild-type parkin. Although wild-type PINK1 localizes in aggregated mitochondria, PINK1 mutants localization remains diffuse and mitochondrial elimination is not observed. This phenomenon is not observed in autophagy-deficient cells. These results suggest that mitophagy controlled by the PINK1/parkin pathway might be associated with PD pathogenesis.

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