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Reactivation of Zeta-Globin by deletion of BCL11A and LRF in HUDEP cells (ATAC-seq)

ABSTRACT: The alpha and beta-globin loci harbour genes that are expressed during development and silenced throughout post-natal life. Learning to reactivate these genes may offer new therapeutic approaches for the hemoglobinopathies, the most common single gene disorders. Here, we address the mechanisms underlying the regulation of the gene encoding zeta-globin, the embryonically expressed alpha-like globin.

ORGANISM(S): Homo sapiens

PROVIDER: GSE173416 | GEO | 2021/04/28

REPOSITORIES: GEO

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Reactivation of Zeta-Globin by deletion of BCL11A and LRF in HUDEP cells (ChIP-seq)

Project description:The alpha and beta-globin loci harbour genes that are expressed during development and silenced throughout post-natal life. Learning to reactivate these genes may offer new therapeutic approaches for the hemoglobinopathies, the most common single gene disorders. Here, we address the mechanisms underlying the regulation of the gene encoding zeta-globin, the embryonically expressed alpha-like globin.

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Reactivation of Zeta-Globin by deletion of BCL11A and LRF in HUDEP cells

Project description:This SuperSeries is composed of the SubSeries listed below.

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Regulation of alpha-like globin gene expression in murine primitive erythropoiesis (NG CaptureC)

Project description:Haemoglobin, the oxygen-carrying molecule of red blood cells, at all stages of development comprises a tetramer of two α-like and two β-like globin chains. In humans and mice the highly conserved α- and β-globin loci contain genes encoding globin chains specifically expressed only during the first trimester of gestation (termed embryonic globins) in addition to the genes encoding globin chains expressed throughout adult life. In humans the β-globin locus also encodes a β-like chain that is expressed throughout the second and third trimesters of development; this is termed γ-globin and complexes with α-globin to form fetal haemoglobin (HbF). The sequential activation and repression of the genes at each of these loci throughout development to maturity is termed haemoglobin switching and is a poorly understood process. α-thalassemia, which results from insufficient production of α-globin, is a major global health problem with several hundred thousand sufferers world-wide. The embryonically expressed ζ-globin, encoded by the gene HBZ (Hba-x in mice), can functionally substitute for α-globin in adult erythroid cells. Reactivation of this gene is consequently likely to ameliorate the symptoms of α-thalassemia in individuals with a severe phenotype. Little is currently known about the regulation of ζ-globin expression in terms of both the trans- and cis-acting regulatory elements responsible for high-levels of expression of this gene during embryonic erythropoiesis and its maintenance in a transcriptionally inactive state throughout adult life. Using ATACseq and NG Capture C and mutant mouse lines this work aims to identify and define the cis-acting regulatory network underlying zeta-globin expression, and define the contribution of each regulatory element.

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