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Figure 4 | BMC Genomics

Figure 4

From: Analysis of the peroxisome proliferator-activated receptor-β/δ (PPARβ/δ) cistrome reveals novel co-regulatory role of ATF4

Figure 4

Characterization of PPARβ/δ binding on chromatin in keratinocytes. (A) ChIP-seq analysis was performed to identify regions of chromatin with PPARβ/δ occupancy (Hotspot analysis). These data were filtered to correct for background by removing peaks detected in Pparβ/δ-null samples and to identify peaks within a ± 10 kb region of any transcription start site (TSS). These filtered data were then compared with expression levels of genes to identify direct PPARβ/δ target genes that were regulated with and without exogenous ligand (B) Annotation of ChIP-seq peaks with chromosome localization. The percentage of the mouse genome on each chromosome is shown in relationship to the percentage of the ChIP-seq peaks detected that were localized to each chromosome. (C) Annotation of ChIP-seq peaks either upstream or downstream from TSS. The percentage of the ChIP-seq peaks detected that were localized between 1000 and 3000 bp from the TSS is shown as compared to the percentage of the mouse genome in these regions. (D) Annotation of ChIP-seq peaks in the intragenic 5′-UTR, 3′-UTR, coding exons and introns. The percentage of the ChIP-seq peaks detected in intragenic 5′-UTR, 3′-UTR, coding exons and introns is shown as compared to the percentage of the mouse genome in these regions. *Significantly different from respective genomic control, P ≤ 0.05 as determined by ANOVA and post-hoc testing.

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