Genomics

Dataset Information

98

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

REPOSITORIES: GEO

altmetric image

Publications


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]

Similar Datasets

2016-01-07 | E-GEOD-74371 | ArrayExpress
2009-09-10 | GSE18042 | GEO
2009-11-25 | GSE18870 | GEO
2009-09-18 | E-GEOD-18042 | ArrayExpress
2013-03-04 | E-GEOD-43356 | ArrayExpress
2008-02-05 | GSE10134 | GEO
2008-02-05 | E-GEOD-10134 | ArrayExpress
2010-09-25 | GSE24336 | GEO
2010-09-25 | GSE24333 | GEO
| GSE60137 | GEO