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Fig. 1 | Genome Biology

Fig. 1

From: GATA3-dependent cellular reprogramming requires activation-domain dependent recruitment of a chromatin remodeler

Fig. 1

Chromatin domain bound by GATA3 becomes more accessible together with increased levels of enhancer-like histone marks. a Genomic localization of GATA3 across three breast cancer cell lines. UCSC Genome Browser snapshot showing the mapped read coverage of GATA3 ChIP-seq in MDA-MB-231 (blue), MCF7 (green), and T47D cells (red). The top motif identified by HOMER de novo motif analysis is represented at the right with P values. b Representative genomic loci acquired DNA accessibility. The GATA3-binding sites displayed: (top) significant increased level or (bottom) de novo peaks of ATAC-seq, H3K4me1, and H3K27ac signals after ectopic expression of GATA3. The other example loci are shown in Additional file 1: Figure S1. Metagene profiles of normalized ATAC-seq (c), H3K4me1 ChIP-seq (d), and H3K27ac ChIP-seq (e) are shown to compare the average signal levels centered on GATA3 ChIP-seq peaks in control and GATA3 expressing cells. The GATA3 peaks are divided into TSS-proximal (less than or equal to 1 kb) or distal (more than 1 kb) peaks based on the distance

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