Mitochondria dysfunction is considered as a hallmark of multiple neurodegenerative diseases,such as Parkinsons disease (PD).Mutations in two PD related genes, PTEN-induced kinase 1 (Pink1;PARK6), a mitochondrial serine-threonine kinase, and parkin (PARK2), an E3 ligase,can impair mitochondrial function.Our previous results showed that Pink1 acts upstream of parkin in a common genetic pathway to promote mitochondrial fi ssion or inhibit fusion in Drosophila (Deng et al., 2008).Indeed, mfn, a fusion molecule on the mitochondria outer membrane, was proved to be a substrate of parkin for ubiquitination and degradation (Ziviani et al., 2010).Accumulative evidence from mammalian cell culture suggested that pink1/parkin pathway also function in a process called mitophagy (mitochondrial selective autophagy) (Chan and Chan, 2011;Youle and Narendra, 2011).Mitophagy through mitochondrial fission and lysosomal recycling was considered as a mitochondrial quality control system in organelle level.However, the physiological role of these processes on cellular health and tissue maintenance is still elusive.We hypothesized that enhancing the auto-lysosomal clearance of dysfunctional mitochondria may be beneficial for pink1 and parkin mutants in Drosophila.Indeed, we found over-expression of atg1, a highly conserved kinase that initiate and induce autophagosome formation, can signifi cantly rescue the mitochondrial defects and the apoptotic cell death in pink1 and parkin mutants.Surprisingly, we found the rescue effect relied on both the intact endosome-lysosome machinery and also on drp1, a mitochondrial fission molecule.We further demonstrated that Atg1 can promote mitochondrial fi ssion by post-transcriptionally transcriptionally increase drp1 protein level.On the other hand, Atg1 is indispensable for mitochondrial fission associated suppression on pink1/parkin mutants.