Fig. 3
From: An HDAC3-PROX1 corepressor module acts on HNF4α to control hepatic triglycerides
The HDAC3–PROX1 module is recruited by HNF4α in liver. a Comparison of HNF4α binding (>2 rpm, filtered on the HNF4α KO, 50% minimum overlap) at overlapping and non-overlapping peaks in the HDAC3 and PROX1 cistromes from Fig. 2a. Numbers above brackets indicate P-values, χ 2 test. b HOMER motif analysis of peaks co-bound by HDAC3, PROX1, and HNF4α displaying over-represented sequences. c Representative browser tracks of HNF4α, PROX1, and HDAC3 ChIP-seq in Hnf4α fl/fl livers infected with AAV8 TBG Egfp (Ctl) or Cre (Hnf4α KO). Indicated scales are in RPTM. d Scatter plots of PROX1 (left) and HDAC3 (right) ChIP-seq in control versus Hnf4α KO. Red and blue shaded regions indicate a twofold decrease in peak intensity upon loss of HNF4α. e, f Co-occupancy of HDAC3–PROX1 and HNF4α as indicated by ChIP–reChIP (n = 3) from liver. Legend indicates reChIP antibody following primary HDAC3 or PROX1 ChIP elution. Data are presented as mean ± s.d, one-tailed unpaired Student’s t-test, *P < 0.05, **P < 0.01, ***P < 0.001, ns not significant
