The study investigates the role of PINK1-dependent recruitment of Parkin to mitochondria in mitophagy. It demonstrates that the relocation of Parkin to mitochondria upon mitochondrial membrane potential (ΔΨm) collapse relies on PINK1 expression. Overexpression of wild-type (WT) but not mutated PINK1 causes Parkin translocation to mitochondria, even in cells with normal ΔΨm. Co-overexpression of Parkin and PINK1 leads to the formation of mitochondrial aggregates and perinuclear clusters surrounded by autophagic vacuoles. The results suggest that Parkin and PINK1 modulate mitochondrial trafficking, particularly to the perinuclear region, where damaged mitochondria are degraded by autophagy. Mutations in either Parkin or PINK1 impair this process, potentially leading to neurodegeneration in Parkinson's disease.The study investigates the role of PINK1-dependent recruitment of Parkin to mitochondria in mitophagy. It demonstrates that the relocation of Parkin to mitochondria upon mitochondrial membrane potential (ΔΨm) collapse relies on PINK1 expression. Overexpression of wild-type (WT) but not mutated PINK1 causes Parkin translocation to mitochondria, even in cells with normal ΔΨm. Co-overexpression of Parkin and PINK1 leads to the formation of mitochondrial aggregates and perinuclear clusters surrounded by autophagic vacuoles. The results suggest that Parkin and PINK1 modulate mitochondrial trafficking, particularly to the perinuclear region, where damaged mitochondria are degraded by autophagy. Mutations in either Parkin or PINK1 impair this process, potentially leading to neurodegeneration in Parkinson's disease.