Mitophagy　is　the　selective　degradation　of　mitochondria　by　autophagy,　which　is　an　important　mitochondrial　quality　and　quantity　control　process.　During　Drosophila　metamorphosis,　the　degradation　of　midgut　involves　a　large　change　in　length　and　organization,　which　is　mediated　by　autophagy.　Here　we　noticed　a　cell-type　specific　mitochondria]　clearance　process　that　occurs　in　enterocytes　(ECs),　while　most　mitochondria　remain　in　intestinal　stem　cells　(ISCs)　during　metamorphosis.　Although　PINK]/PARKIN　represent　the　canonical　pathway　for　the　elimination　of　impaired　mitochondria　in　varied　pathological　conditions,　their　roles　in　developmental　processes　or　normal　physiological　conditions　have　been　less　studied.　To　examine　the　potential　contribution　of　PINK1　in　developmental　processes,　we　monitored　the　dynamic　expression　pattern　of　PINKI　in　the　midgut　development　by　taking　advantage　of　a　newly　CRISPR/Cas9　generated　knock-in　fly　strain　expressing　PINK1-mCherry　fusion　protein　that　presumably　recapitulates　the　endogenous　expression　pattern　of　PINK1.　We　disclosed　a　spatiotemporal　correlation　between　the　expression　pattern　of　PINKI　and　the　mitochondrial　clearance　or　persistence　in　ECs　or　ISCs　respectively.　By　mosaic　genetic　analysis,　we　then　demonstrated　that　PINK1　and　PARKIN　function　epistatically　to　mediate　the　specific　timely　removal　of　mitochondria,　and　are　involved　in　global　autophagy　in　ECs　during　Drosophila　midgut　metamorphosis,　with　kinase-dead　PINKI　exerting　dominant　negative　effects.　Taken　together,　our　studies　concluded　that　the　PINK1/PARKIN　is　crucial　for　timely　cell-type　specific　mitophagy　under　physiological　conditions　and　demonstrated　again　that　Drosophila　midgut　metamorphosis　might　serve　as　an　elegant　in　vivo　model　to　study　autophagy.　(C)　2016　Elsevier　Inc.　All　rights　reserved.