Dataset Information


ATAC-seq reveals GATA-1- and heme-dependent chromatin targeting in erythroid cells.

ABSTRACT: CRISPR/Cas9-mediated ablation of two Alas2 intronic cis-elements in G1E-ER-GATA1 cells strongly reduced GATA-1-induced Alas2 transcription, heme biosynthesis, and GATA-1 regulation of other vital constituents of the erythroid cell transcriptome. Bypassing Alas2 function in Alas2 cis-element-mutant (double mutant) cells by providing its catalytic product 5-aminolevulinic acid (5-ALA) rescued heme biosynthesis and a subset of GATA-1-dependent genetic network. Using the same system, we discovered a GATA-1- and heme-dependent circuit that regulates chromatin accessibility during erythroid maturation. Overall design: G1E-ER-GATA1 WT and double mutant cells were examined. Untreated WT, beta-estradiol-treated WT, untreated double mutant, beta-estradiol-treated double mutant and beta-estradiol/5-ALA-treated double mutant cells were subject to ATAC-seq.

INSTRUMENT(S): Illumina NextSeq 500 (Mus musculus)

SUBMITTER: Emery H. Bresnick  

PROVIDER: GSE114996 | GEO | 2018-05-30


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By functioning as an enzyme cofactor, hemoglobin component, and gene regulator, heme is vital for life. One mode of heme-regulated transcription involves amplifying the activity of GATA-1, a key determinant of erythrocyte differentiation. To discover biological consequences of the metal cofactor-transcription factor mechanism, we merged GATA-1/heme-regulated sectors of the proteome and transcriptome. This multi-omic analysis revealed a GATA-1/heme circuit involving hemoglobin subunits, ubiquitin  ...[more]

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