Fig. 7.

Erg1 regulates FAO transcription via Nab1-dependent recruitment of HDACs.

(A–D) HepaRG cell were transduced with Ad-Egr1, Ad-Egr1Δ, or Ad-GFP followed by treatment with GW7647 (0.1 μM). ChIP assays were performed with anti-acetyl H3K9 (A), anti-acetyl H3K14 (B), anti-acetyl H3K18 (C), and anti-acetyl H3K27 (D). N = 3 biological replicates. Data are expressed as mean ± SD. ∗p <0.05, one-way ANOVA with the post hoc Scheffé test. (E) HepaRG cell were transduced with Ad-Egr1 or Ad-GFP followed by treatment with GW7647 (0.1 μM) in the presence or absence of two pan-HDAC inhibitors (panobinostat [0.1 μM] and pracinostat [0.5 μM]). FAO genes were examined by qPCR. N = 3 biological replicates. Data are expressed as mean ± SD. ∗p <0.05, one-way ANOVA with the post hoc Scheffé test. Ad-Egr1, adenovirus carrying Egr1; Ad-Egr1Δ, adenovirus carrying Egr1 mutant; Ad-GFP, adenovirus carrying a control vector; ChIP, chromatin immunoprecipitation; Erg1, early growth response 1; FAO, fatty acid oxidation; GFP, green fluorescent protein; HDAC, histone deacetylase; Nab1, NGFI-A binding protein 1; PPAR, peroxisome proliferator-activated receptor; PPRE, PPAR response element; qPCR, quantitative PCR.