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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 7. MiroS156A Prevents Mitochondrial Arrest by PINK1/Parkin Overexpression in Rat Hippocampal Axons.

Figure 7

(A,B) Expression of PINK1-Flag (A) or YFP-Parkin (B) at a 3:1 ratio to wild type Miro arrested mitochondria. (C,D) Expression of PINK1-Flag (C) or YFP-Parkin (D) at a 3:1 ratio to MiroS156A did not arrest mitochondria. (E) From kymographs as in (A–D), the percent of time each mitochondrion was in motion was determined and averaged (n=85–153 mitochondria from 8 axons and 4 separate transfections per genotype). (F) Schematic representation of the proposed mechanism of PINK1/Parkin-dependent mitochondrial arrest. Mitochondrial depolarization stabilizes PINK1 on the surface of the mitochondrion, promotes its interaction with Miro, and causes PINK1 to phosphorylate Ser156 of Miro. Subsequent interaction of Parkin with Miro and likely ubiquitination causes Miro to be removed from the membrane and degraded by the proteasome, releasing milton and kinesin from the organelle. Scale bars, 10 µm. See also Figure S6 and Table S4.