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. Author manuscript; available in PMC: 2015 Oct 29.
Published in final edited form as: Cell. 2014 May 8;157(4):882–896. doi: 10.1016/j.cell.2014.03.026

Figure 3. XPA deficiency impairs cellular mitophagy and sensitizes cells to caspase-9 regulated apoptosis under multiple mitochondrial stresses.

Figure 3

(A) Cells were treated with mitochondrial toxins for 24 h, and LC3 was detected by immunoblot in total cell lysates. Rotenone: a mitochondrial complex I inhibitor, antimycin A: a mitochondrial complex III inhibitor, FCCP: a mitochondrial uncoupler. (B) Quantitative values of relative LC3-II levels normalized to Actin (means ± S.D., n=3). (C) Relative values of mitochondrial content in XPA− and XPA+ cells after different treatments using flow cytometry (means ± S.D., n=3). (D, E) Quantification of colocalization of LC3 and p62 (D) or COX4 and p62 (E) after treatment with mitochondrial toxins as determined by Pearson’s correlation coefficient using confocal microscopy (means ± S.E.M., n>50). See also Figure S4A and S4B. (F) Detection of apoptosis using flow cytometry in XPA− and XPA+ cells with Annexin-V/PI staining after mitochondrial stressors. Quantification is shown on the right (means ± S.D., n=3). (G) Immunoblot of the expression of proteins involved in caspase-8 regulated and caspase-9 regulated apoptotic pathways in XPA− and XPA+ cells exposed to different mitochondrial toxins. See also Figure S4.