Parkinsons Disease (PD) is a common neurodegenerative disorder caused by selective loss of dopaminergic neurons in the substantia nigra.Genetic studies on familial forms of PD have led to the identification of six PD genes,but their biochemical functions are not clear.To dissect the defective molecular pathways in PD patients,we have generated Drosophila mutants for PTEN-induced kinase 1 (Pink1),a PD gene encoding a putative mitochondrial ser/thr kinase.Loss of Pink1 function causes male sterility,apoptotic muscle degeneration and increased sensitivity to oxidative stress.These phenotypes were accompanied by severe morphological defects in mitochondria.Overexpression of another PD gene,Parkin,rescues Pinkl mutant phenotypes and mitochondrial defects,suggesting that Parkin functions downstream of Pink1.These results implicate mitochondrial dysfunction as a key event in PD pathogenesis.