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. 2021 Jan 26;17(8):2011–2036. doi: 10.1080/15548627.2021.1874133

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© 2021 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License (http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited, and is not altered, transformed, or built upon in any way.

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Figure 5. — BCAS3 colocalizes with autophagy proteins in response to mitophagy. (A-H) HeLa cells stably expressing 3FLAG-BCAS3 and HA-PRKN (A), 3HA-BCAS3, GFP-ULK1 and GST-PRKN (B), 3HA-BCAS3, GFP-ZFYVE1 and GST-PRKN (C), 3HA-BCAS3, GFP-WIPI1 and GST-PRKN (D), 3HA-BCAS3 and GST-PRKN (E and G), 3HA-BCAS3, 3FLAG-ATG2AC and GST-PRKN (F), and HCT116 cells stably expressing 3FLAG-BCAS3 and HA-PRKN (H) were treated with DMSO or valinomycin for 3 h and then immunostained. Magnified images are shown in the rightmost panels. Bars: 20 µm. (I and J) HeLa cells stably expressing untagged PRKN and the C16orf70-3HA-BCAS3 complex (C16-3HA/BCAS3) using an IRES system were treated with valinomycin for 3 h and then immunostained. The z-stack images were taken with an SP8 confocal microscope and processed for deconvolution and maximum projection. Magnified images are shown to the right. Bars: 10 µm