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. Author manuscript; available in PMC: 2017 Oct 6.
Published in final edited form as: Mol Cell. 2016 Sep 22;64(1):163–175. doi: 10.1016/j.molcel.2016.08.023

Figure 5. IBET 525762A treatment displaces Brd4 from OXPHOS promoters and increases transcription in complex I-deficient cells.

Figure 5

A, ChIP- I-BET 525762A displaces Brd4 from nuclear-encoded mitochondrial promoters. Negative control promoter region Atp1A3 is unaltered. B, ChIP- PGC-1α occupancy increases upon I-BET 525762A-mediated Brd4 displacement. C, ChIP- Brd4 is displaced upon adPGC-1α over-expression. Data is representative of mean ± s.e.m., n=3. Asterisks denote *p<0.05 or **p<0.01 via Student's t-test. D-F, I-BET 525762A-mediated displacement of Brd4 (D) and ablation of Brd4 by CRISPR (E) increases expression of OXPHOS genes while over-expression of Brd4 decreases OXPHOS gene expression (F). Data represents mean ± s.e.m., n=3. Asterisks denote *p<0.05 or **p<0.01 via Student's t-test. G-H, ShPGC-1α KD in ND1-mutated cybrids fail to increase OXPHOS transcripts (G) and partially blunts rescue from galactose-induced cell death (H) when treated with I-BET 525762A. See also Figure S4.