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. Author manuscript; available in PMC: 2012 Nov 11.
Published in final edited form as: Cell. 2011 Nov 11;147(4):893–906. doi: 10.1016/j.cell.2011.10.018

Figure 2. PINK1-dependent Mitochondrial Arrest Requires Parkin.

Figure 2

Mouse hippocampal axons were transfected with mito-dsRed and analyzed with in kymographs, as in Figure 1. (A) A wildtype(Parkin+/+) axon. (B) A Parkin−/− axon in which mitochondrial movement appears normal. (C, D) Expression of PINK1-Flag arrested mitochondria in a wildtype axon (C) but not in a Parkin−/− axon (D). (E, F) Tranfection with 0.5 µg YFP-Parkin DNA per well arrested mitochondria in wildtype (E), but not Parkin−/− (F) axons. (G, H) Tranfection with 0.5 µg YFP-Parkin DNA allowed PINK1 expression to arrest mitochondria in both wildtype (G) or Parkin−/− (H) axons. (I) From kymographs as in (A–H), the percent of time each mitochondrion was in motion was determined and averaged. n=108–157 mitochondria from 8 axons and 4 separate transfections per genotype. (J) Mitochondrial motility as a function of the amount of transfected YFP-Parkin DNA/well of a 24-well plate. n=97–157 mitochondria from 8 axons and 4 separate transfections per genotype. (K) Movies were taken before and after 15 min incubation with 80 µM Antimycin A and analyzed by kymograph (see Figure S2C–D). n=140–174 mitochondria from 8 axons and 8 separate transfections per genotype. Before Antimycin A, Parkin+/+ and Parkin−/− axons did not significantly differ. P values were calculated by comparing a given genotype to its control in (I), to 0 µg Parkin DNA in (J), and by comparing before and after Antimycin A in (K). Scale bars, 10 µm. See also Figure S2, Movies S2 and Table S2.