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Fig. 1 Distinct enhancer binding of CEBPA in WT GMPs versus p30 L-GMPs.
Distinct enhancer binding of CEBPA in WT GMPs versus p30 L-GMPs. (A) Representative examples of CEBPA, H3K4me1, and H3K27Ac ChIP-seq tracks in WT GMPs and Lp30 L-GMPs, showing L-GMP p30-specific CEBPA binding. (B) Distribution of p42-specific, p30-specific, and common CEBPA-bound regions. (C) Normalized intensity tags per million (TPM) of CEBPA (left), H3K4me1 (center), and H3K27ac (right) at midpoint-centered enhancers [rows, ±5000 base pairs (bp)] across the three classes of regions in either WT GMPs or Lp30 L-GMPs. (D) Normalized intensity (TPM) for either H3K4me1 (purple) or H3K27ac (green) across the three classes of regions (midpoint-centered ±500 bp). “Random” represents all regions shuffled randomly across the genome. (E) Distribution of the three classes of regions into LSK-, preGM-, GMP-, and granulocyte-specific enhancers. (F) Subdivision of the three enhancer categories based on whether their nearest-neighbor genes are up- or down-regulated in Lp30 L-GMPs versus WT GMPs (log2 fold change > 0.58, P < 0.05 by edgeR, see Materials and Methods). Statistics are two-sided Fisher’s exact test between groups. ns, not significant. Janus S. Jakobsen et al. Sci Adv 2019;5:eaaw4304 Copyright © 2019 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution NonCommercial License 4.0 (CC BY-NC).
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