1. Spatial Parkin Translocation and Degradation of Damaged Mitochondria via Mitophagy in Live Cortical Neurons 姚溢洲英文学习资料 .pdfVIP

Current Biology 22 , 545–552, March 20, 2012 ª2012 Elsevier Ltd All rights reserved DOI 10.1016/j.cub.2012.02.005 Report Spatial Parkin Translocation and Degradation of Damaged Mitochondria via Mitophagy in Live Cortical Neurons Qian Cai,1,2,* Hesham Mostafa Zakaria,1,3 Anthony Simone,1 vehicle dimethyl sulfoxide (DMSO) as a control, 10 mM and Zu-Hang Sheng1,* carbonyl cyanide m-chlorophenyl hydrazone (CCCP; a Dcm 1Synaptic Functions Section, Porter Neuroscience Research dissipating reagent), or 10 mM CCCP with lysosomal inhibitors Center, National Institute of Neurological Disorders and (LIs; 10 mM pepstatin A and 10 mM E64D). Although YFP-Parkin Stroke, National Institutes of Health, Room 2B-215, was diffuse in the cytosol of DMSO-treated control neurons 35 Convent Drive, Bethesda, MD 20892-3706, USA (n = 435), it redistributed to mitochondria in 26.67% 6 4.46% 2Department of Cell Biology and Neuroscience, Rutgers of neurons (n = 420) treated with CCCP and in 55.87% 6 University, 604 Allison Road, Piscataway, NJ 08854-6999, USA 6.57% of neurons treated with CCCP/LIs (n = 570) (Figures 3Howard Hughes Medical Institute, National Institutes of 1A and 1B). Treatment with CCCP/LIs doubled the percentage Health Research Scholars Program, 1 Cloister Court, of neurons with Parkin translocation relative to CCCP alone Building 60, Bethesda, MD 20814, USA (p 0.001), suggesting that lysosomal degradation capacity has a significant impact on the clearance of Parkin-targete