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Genome-wide maps of chromatin accessibility in C57bl\6 mouse erythroid cells.

ABSTRACT: Genome-wide identification of active regions in the mouse erythroid genome using DNase-seq.

ORGANISM(S): Mus musculus

PROVIDER: GSE49458 | GEO | 2013/11/11

SECONDARY ACCESSION(S): PRJNA214041

REPOSITORIES: GEO

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Genome-wide maps of chromatin accessibility in C57bl\6 mouse erythroid cells.

Project description:Genome-wide identification of active regions in the mouse erythroid genome using DNase-seq. DNAse-seq was performed in C57bl\6 mouse erythroid Ter119+ cells.

2013-11-11 | E-GEOD-49458 | biostudies-arrayexpress

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Genome-wide maps of chromatin modifications in C57bl\6 mouse erythroid cells.

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Project description:We generated genome-wide chromatin state and RNA Polymerase II binding maps in mouse erythroid cells by ChIP-Seq. Examination of 4 different histone modifications (H3K4me3, H3K4me1, H3K27me3, H3K27ac) and RNA Polymerase II (RNAP2) binding in mouse erythroid cells (Ter119+).

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Erythroid lineage chromatin accessibility maps facilitate identification and validation of NFIX as a fetal hemoglobin repressor.

Project description:Human genetics has validated de-repression of fetal gamma globin (HBG) in adult erythroblasts as a powerful therapeutic paradigm in diseases involving defective adult beta globin (HBB)1. To identify factors involved in the switch from HBG to HBB expression, we performed Assay for Transposase Accessible Chromatin with high-throughput sequencing (ATAC-seq)2 on sorted erythroid lineage cells derived from bone marrow (BM) or cord blood (CB), representing adult and fetal states, respectively. BM to CB cell ATAC-seq profile comparisons revealed genome-wide enrichment of NFI DNA binding motifs and increased NFIX promoter chromatin accessibility, suggesting that NFIX may repress HBG. NFIX knockdown in BM cells increased HBG mRNA and fetal hemoglobin (HbF) protein levels, coincident with increased chromatin accessibility and decreased DNA methylation at the HBG promoter. Conversely, overexpression of NFIX in CB cells reduced HbF levels. Identification and validation of NFIX as a new target for HbF activation has implications in the development of therapeutics for hemoglobinopathies.

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