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ATF4 regulates MYB to increase g-globin in response to loss of β-globin [RNA-seq]

ABSTRACT: Boontanrart et al model the cellular stress that occurs upon reduction in β-globin in human erythroid cells. Decrease in β-globin attenuates the eIF2aP-ATF4 pathway and results in upregulating fetal g-globin. Down-regulation of ATF4 leads to decreased levels of the g-globin repressor MYB through direct binding at the HBS1L-MYB intergenic region.

ORGANISM(S): Homo sapiens

PROVIDER: GSE153764 | GEO | 2020/07/26

REPOSITORIES: GEO

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ATF4 regulates MYB to increase g-globin in response to loss of β-globin [ChIP-seq]

Project description:Boontanrart et al model the cellular stress that occurs upon reduction in β-globin in human erythroid cells. Decrease in β-globin attenuates the eIF2aP-ATF4 pathway and results in upregulating fetal -globin. Down-regulation of ATF4 leads to decreased levels of the -globin repressor MYB through direct binding at the HBS1L-MYB intergenic region.

2020-07-26 | GSE153767 | GEO

ATF4 regulates MYB to increase g-globin in response to loss of β-globin

Project description:ATF4 regulates MYB to increase g-globin in response to loss of β-globin

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ATF4 regulates MYB to increase g-globin in response to loss of β-globin [ChIP-seq]

Project description:ATF4 regulates MYB to increase g-globin in response to loss of β-globin [ChIP-seq]

| PRJNA643998 | ENA

ATF4 regulates MYB to increase g-globin in response to loss of β-globin [RNA-seq]

Project description:ATF4 regulates MYB to increase g-globin in response to loss of β-globin [RNA-seq]

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HBS1L-MYB intergenic variants modulate fetal hemoglobin via long-range MYB enhancers

Project description:Genetic studies have identified common variants within the HBS1L-MYB intergenic region on chromosome 6q associated with elevated fetal hemoglobin (HbF) levels and other clinically important human erythroid traits. The mechanism by which the non-coding sequence variants affect these traits is still not clear. Here we report that several of the variants affect regulatory elements that are occupied by key erythroid transcription factors within this region. These elements interact with MYB, a critical regulator of erythroid development and HbF levels. We show that several of the variants reduce transcription factor binding, affecting long-range interactions with MYB, and MYB expression levels. We provide here a functional explanation for the genetic association of HBS1L-MYB intergenic polymorphisms with human erythroid traits and HbF levels. Our results further designate MYB as a bona fide target for therapeutic induction of HbF to ameliorate sickle cell and β-thalassemia disease severity.

2014-07-24 | GSE52637 | GEO

ATF4 regulates MYB to increase g-globin in response to loss of β-globin

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

2020-07-26 | GSE153768 | GEO

HRI activates ATF4 to promote BCL11A transcription and fetal hemoglobin silencing [ChIP-seq]

Project description:Through a CRISPR-Cas9 guided loss-of-function screen in human erythroid cells we identified transcription factor ATF4, a known HRI-regulated protein, as a novel γ-globin repressor. ATF4 binds to a BCL11A enhancer to augment promoter contacts, stimulates BCL11A transcription to repress γ-globin expression. Notably, mice deficient for HRI displayed normal Bcl11a levels, suggesting species selective regulation that we explain here by demonstrating that the analogous ATF4 motif at the murine Bcl11a enhancer is largely dispensable. This illustrates potential limits of commonly used murine models of globin gene regulation.

2020-04-17 | GSE143961 | GEO

HRI activates ATF4 to promote BCL11A transcription and fetal hemoglobin silencing [Capture-C]

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Expression Profiling of Erythroid Progenitors After MYB shRNA Knockdown

Project description:MYB plays a critical role as a regulator of erythropoieisis. We have shown that MYB silences epsilon and gamma-globin expression in erythroid progenitors. We here examine erythroid cells at the basophilic erythroblast stage of differentiation with MYB shRNA or control lentiviral transduction prior to differentiation.

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Disrupting the adult-globin promoter alleviates promoter competition and reactivates foetal-globin gene expression

Project description:The benign condition Hereditary Persistence of Foetal Haemoglobin (HPFH) is known to ameliorate symptoms when co-inherited with beta-haemoglobinopathies, such as sickle cell disease and beta-thalassaemia. The condition is sometimes associated with point mutations in the foetal globin promoters that disrupt the binding of the repressors BCL11A or ZBTB7A/LRF, which have been extensively studied. HPFH is also associated with a range of deletions within the beta-globin locus that all reside downstream of the foetal HBG2 gene. These deletional forms of HPFH are poorly understood and are the focus of this study. Numerous different mechanisms have been proposed to explain how downstream deletions can boost the expression of the foetal globin genes, including the deletion of silencer elements, of genes encoding non-coding RNA, and bringing downstream enhancer elements into proximity with the foetal globin gene promoters. Here we systematically analyse the deletions associated with both HPFH and a related condition known as beta-thalassaemia and propose a unifying mechanism. In all cases where foetal globin is up-regulated, the proximal adult beta-globin (HBB) promoter is deleted. We use CRISPR gene editing to delete or disrupt elements within the promoter and find that virtually all mutations that reduce promoter activity, result in elevated foetal globin expression. These results fit with previous models where the foetal and adult globin genes compete for the distal Locus Control Region and suggest that targeting the promoter might be explored to elevate foetal globin and reduce sickle globin expression as a treatment for beta-haemoglobinopathies.

2022-01-20 | GSE194064 | GEO

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