Distinct Ldb1/NLI complexes orchestrate γ-globin repression and re-activation through ETO2 in human adult erythroid cells.
Source: NCBI BioProject (ID PRJNA144083)

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Project name: Homo sapiens
Description: The Ldb1/GATA-1/TAL1/LMO2 complex mediates long range interaction between the β-globin locus control region (LCR) and gene in adult mouse erythroid cells but whether this complex mediates chromatin interactions at other developmental stages or in human cells is unknown. We investigated human NLI (Ldb1 homologue) complex occupancy and chromatin conformation of the β-globin locus in human erythroid cells. In addition to the LCR, we find robust NLI complex occupancy at a site downstream of the Aγ-globin gene, within sequences of BGL3, an intergenic RNA transcript. In cells primarily transcribing β-globin, BGL3 is not transcribed and BGL3 sequences are occupied by NLI core complex members together with co-repressor ETO2 and γ-globin repressor BCL11A. The LCR and β-globin gene establish proximity in these cells. In contrast, when γ-globin transcription is re-activated by cytokines in these cells, ETO2 participation in the NLI complex at BGL3 is diminished, as is BCL11A occupancy, and both BGL3 and γ-globin are transcribed. In these cells, proximity between the BGL3/γ-globin region and the LCR is established. Thus, alternative NLI complexes mediate γ-globin transcription or silencing through long range LCR interactions involving an intergenic site of non-coding RNA transcription and ETO2 is critical to this process.ChIP-chip of GATA-1, NLI, and pol II in cell linesOverall design: Comparison of GATA-1, NLI, and pol II binding on chromatin. 2 replicates for each protein; ChIP and input DNA for each replicate
Data type: Epigenomics
Sample scope: Multiisolate
Relevance: Medical
Organization: Laboratory of Cellular and Developmental Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health
Literatures
  1. PMID: 22010104
Release date: 2012-01-05
Last updated: 2011-06-17