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Fig. 4 | Epigenetics & Chromatin

Fig. 4

From: Affinity-seq detects genome-wide PRDM9 binding sites and reveals the impact of prior chromatin modifications on mammalian recombination hotspot usage

Fig. 4

Affinity-seq and H3K4me3 peak strength in closed vs. open chromatin. a Density plots of H3K4me3 signals in closed versus open chromatin as determined by the absence or presence of H3K9me2/3 enrichment reveal that H3K4me3 signals are stronger at hotspots in open chromatin (blue) than in closed chromatin (red). In this analysis, DMC1 hotspots overlapping promoters were excluded. In all three panels, in order to eliminate effects of filtering multi-mapped reads only peaks which span regions of 100 % uniqueness in mappability were selected. Mann–Whitney test gives a p value <2.2 × 10−16 that distributions are the same. b PRDM9 ChIP peaks are found at the sites with strongest affinity to DNA in vitro. Density plots are shown for Affinity-seq read counts normalized to parts per million at peaks for those sites detected by PRDM9 ChIP assay (red) and all sites (blue). Mann–Whitney test gives a p value <2.2 × 10−16 that distributions are the same. c Stronger affinities to DNA are detected at PRDM9 ChIP-seq peaks found in closed compared to open chromatin. Density plots are shown for Affinity-seq read counts normalized to parts per million at peaks in H3K9me2/3 enriched regions (red) and peaks at regions not enriched for H3K9me2/3 (blue). Mann–Whitney test gives a p value <2.2 × 10−16 that distributions are the same

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