Figure 13. MITOL∆C8 ubiquitylates expanded peroxisomes following CCCP treatment.

• A, B
  HeLa cells expressing HA‐Parkin and MITOL∆C8 (A) or MITOL∆C8 lacking E3 activity (B) were treated with 15 μM CCCP for 3 h, and then subjected to immunocytochemistry with anti‐Flag and anti‐ubiquitin antibodies. Expanded peroxisomes were ubiquitylated upon E3 activity of MITOL. Higher magnification images of the boxed regions are shown in the small panel. Scale bars, 10 μm.
• C
  The schematic model of PINK1/Parkin‐mediated MITOL redistribution. MITOL is targeted to mitochondria with sustained membrane potential via Tom70. In response to mitophagy stimuli, Parkin‐catalyzed ubiquitylation of MITOL causes its extraction from damaged mitochondria in a p97/VCP‐dependent manner, and then, MITOL translocates to peroxisomes via Pex3/Pex16 pathway. As ubiquitylation of MITOL is rarely observed in the absence of NMS‐873, MITOL inserted into the peroxisome membrane is shown here in the non‐ubiquitylated form.