Fig. 5: The PPARγ1 K154/155 residues govern relative DNA-sequence-specific binding to canonical vs. non-canonical sequences in chromatin. | Oncogene

Fig. 5: The PPARγ1 K154/155 residues govern relative DNA-sequence-specific binding to canonical vs. non-canonical sequences in chromatin.

From: PPARγ acetylation governs mammary adenocarcinoma tumor growth via acetylated residues that determine DNA sequence-specific binding

Fig. 5: The PPARγ1 K154/155 residues govern relative DNA-sequence-specific binding to canonical vs. non-canonical sequences in chromatin.

A ChIP-Seq analysis was performed on samples derived from MCF10A-NeuT transduced with either PPARγ1 WT or PPARγ1 K154/155Q mutant, and peak calling defined by MACS2 software is shown in the Venn diagram. B Quantitative analysis of PPARγ1 ChIP-Seq signal. Normalized read density is shown in blue for PPARγ WT and in green for PPARγ 154/155Q. Scatterplots of the maximum stack height (tag counts) at each PPARγ1 peak, color-coded based on whether each peak was called alone in PPARγ1 WT or in PPARγ1 K154/155Q or common to both PPARγ1 WT and PPARγ1 K154/155Q. C Distribution of PPARγ1 WT or PPARγ1 K154/155Q peaks relative to the TSS. The region upstream from the TSS was divided as indicated. D Comparison of the enrichment of PPARγ1 WT alone or PPARγ1 K154/155Q for each canonical or non-canonical PPARγ1 motif. E Comparison of the percentage of peaks within PPARγ1 WT alone or PPARγ1 K154/155Q for each PPARγ1 motif. F The -fold enrichment (observed/expected) for PPARγ1 WT or PPARγ1 K154/155Q at CEBP sites defined in MCF7 cells. G–I Integrated genome browser visualization of tag density profiles for ChIP-Seq PPARγ1 WT and K154/155Q. Selected genes are: LSM12, NTNG1 and ABACB.

Back to article page