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. 2016 Aug 10;7:12376. doi: 10.1038/ncomms12376

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Copyright © 2016, The Author(s)

This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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(a) MAnorm analysis of ATAC-sequencing(ATAC-seq) data in control pre-B cells and control bone marrow myeloid (Mac1⁺Gr1⁺) revealed that the accessibility of regulatory sites in lineage-specific genes is differentially (ratio≥4, P value≤0.01) regulated in these two populations. (b) MAnorm analysis of ATAC-seq data in control and Mef2c-deficient pre-B cells revealed that MEF2C is required to promote chromatin accessibility in regulatory regions of genes required for B-cell differentiation. (c) Loss of Mef2c reduced the chromatin accessibility nearby genes that are critical for B-cell differentiation and DNA repair. Many of these regulatory sites are also uniquely accessible in pre-B cells as compared with myeloid cells. Regions that are significantly (ratio≥4, P value≤0.01) more accessible in control than Mef2c-deficient pre-B cells are highlighted in grey and labelled with reference numbers co-related to Supplementary Data 4. Regions that are bound by MEF2C are highlighted in brown. MEF2C bindings that do not yield statistical significance are labelled with asterisks. (d) The ATAC-seq peaks that are more accessible in control pre-B cells compared with Mef2c-deficient pre-B cells are enriched for E-box and EBF motifs. (e) Venn diagram showing extensive overlap of regions that are more accessible in control pre-B cells vs. Mef2c-deficient pre-B cells with regions that are more accessible in pre-B cells than myeloid cells, as well as TCF3-bound regions in pro-B cells.