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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 9. — Loss of the BCAS3-C16orf70 complex does not affect overall mitochondrial degradation in response to mitophagy. (A) WT and BCAS3^-/-C16orf70^-/- DKO clones #1-1-7 and #1-1-17 HCT116 cells stably expressing YFP-PRKN and mt-Keima were treated with DMSO or antimycin A and oligomycin (AO) for 9 h and then analyzed by FACS. Representative FACS data with the percentage of cells exhibiting lysosomal mt-Keima signals are shown. (B) Quantification of the FACS-based mitophagy in (A). Each dot represents the mean value and error bars represent mean ± s.d. in three independent experiments. Statistical differences were determined by student’s t-test (n.s.: not significant)