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

ABSTRACT: Reactivation of Zeta-Globin by deletion of BCL11A and LRF in murine cells

PROVIDER: PRJNA728355 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14472366_1.fastq.gz	Fastqsanger.gz
	SRR14472366_2.fastq.gz	Fastqsanger.gz
	SRR14472367_1.fastq.gz	Fastqsanger.gz
	SRR14472367_2.fastq.gz	Fastqsanger.gz
	SRR14472368_1.fastq.gz	Fastqsanger.gz

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

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

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

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

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

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

| PRJNA725485 | ENA

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

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.

2021-05-09 | GSE174110 | GEO

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

2021-04-28 | GSE173417 | GEO

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

2021-04-28 | GSE173416 | GEO

The LRF/ZBTB7A transcription factor is a BCL11A-independent repressor of fetal hemoglobin

Project description:Hemoglobinopathies, including sickle cell disease and _-thalassemia, are global public health concerns. Induction of fetal-type hemoglobin (HbF) is a promising means to treat these disorders; however, precisely how HbF expression is silenced in adult erythroid cells is not fully understood. Here, we show that the LRF/ZBTB7A transcription factor is a potent repressor of HbF production. LRF inactivation derepresses embryonic/fetal _-globin expression in mouse and human adult erythroid cells. We employed genome-wide analysis of the transcriptome, chromatin accessibility and LRF occupancy sites, and demonstrate that LRF occupies the _-globin loci and maintains nucleosome density necessary for _-globin silencing. LRF confers its repressive activity through a unique NuRD repressor complex independent of BCL11A. Strikingly, human erythroid lines lacking both LRF and BCL11A exhibited almost a complete switch in expression from adult- to fetal-type globin, suggesting that these two factors cumulatively represent the near entirety of _-globin repressive activity in adult erythroid cells. RNA-seq, LRF ChIP-seq and ATAC-seq assays were used to investigtae LRF binding, effect of LRF depletion on transcription and chromatin landscape in mouse and human cells.

2016-01-15 | E-GEOD-74977 | biostudies-arrayexpress

The LRF/ZBTB7A transcription factor is a BCL11A-independent repressor of fetal hemoglobin

2016-01-15 | GSE74977 | GEO

Natural regulatory mutations elevate fetal globin via disruption of BCL11A or ZBTB7A binding

Project description:B-hemoglobinopathies such as Sickle Cell Disease (SCD) and b-thalassemia result from mutations in the adult b-globin gene. Reactivating the developmentally silenced fetal g-globin gene is a therapeutic goal for treating SCD and b-thalassemia1. Some forms of Hereditary Persistence of Fetal Hemoglobin (HPFH), a rare benign condition in which individuals express g‑globin throughout adulthood, are caused by point mutations in the g‑globin gene promoter at regions residing ~115 and 200 base pairs upstream of the transcription start site. Here we show that the major fetal globin repressors BCL11A and ZBTB7A/LRF directly bind to the -115 and ‑200 sites, respectively. Furthermore, introduction of naturally occurring HPFH mutations into erythroid cells by CRISPR/Cas9 disrupts repressor binding and raises g‑globin expression. These findings resolve the mystery surrounding how these HPFH mutations operate and demonstrate that BCL11A and ZBTB7A/LRF are major direct repressors of the fetal globin gene.

2018-01-29 | GSE103445 | GEO

KLF1 directly activates expression of the novel fetal globin repressor, ZBTB7A/LRF, in erythroid cells

Project description:Genes encoding the human β-like hemoglobin proteins undergo a developmental switch from fetal γ-globin to adult β-globin expression at around the time of birth. β-hemoglobinopathies, such as sickle cell disease and β-thalassemia, result from mutations affecting the adult β-globin gene. The only treatment options currently available carry significant side-effects. Analyses of heritable variations in fetal hemoglobin (HbF) levels have provided evidence that reactivation of the silenced fetal γ-globin genes in adult erythroid cells is a promising therapy. The γ-globin repressor BCL11A has become the major focus with several studies investigating its regulation and function as a first step to inhibiting its expression or activity. However, a second repression mechanism has recently been shown to be mediated by the transcription factor ZBTB7A/LRF, suggesting that understanding the regulation of ZBTB7A may also be useful. Here we show that KLF1 directly drives expression of ZBTB7A in erythroid cells by binding to its proximal promoter. We have also uncovered an erythroid-specific regulation mechanism, leading to the upregulation of a novel ZBTB7A transcript in the erythroid compartment. The demonstration that ZBTB7A, like BCL11A, is a KLF1 target gene also fits with the observation that reduced KLF1 expression or activity is associated with HbF derepression.

2017-04-13 | GSE97671 | GEO

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