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Recombinant erythroid Kruppel-like factor fused to GATA1 up-regulates delta- and gamma-globin expression in erythroid cells primary adult human erythroid progenitor cells

ABSTRACT: Recombinant erythroid Kruppel-like factor fused to GATA1 up-regulates delta- and gamma-globin expression in erythroid cells primary adult human erythroid progenitor cells

PROVIDER: PRJNA782320 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16993388.fastq.gz	Fastqsanger.gz
	SRR16993389.fastq.gz	Fastqsanger.gz
	SRR16993390.fastq.gz	Fastqsanger.gz
	SRR16993391.fastq.gz	Fastqsanger.gz
	SRR16993392.fastq.gz	Fastqsanger.gz

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Recombinant erythroid Kruppel-like factor fused to GATA1 up-regulates delta- and gamma-globin expression in erythroid cells primary adult human erythroid progenitor cells

Project description:The EKLF-GATA1 fusion proteins enhances δ-globin expression through interaction with the GATA1-binding motif of the δ-globin promoter. The goal this study is to find if the fusion proteins could have a different pattern of chromatin occupation from GATA1. The alignment of ChIP-Seq peaks revealed that the binding peaks of EKLF-GATA1 fusion proteins at the β-globin cluster overlapped substantially with those of GATA1 (A), suggesting that these proteins may associate with chromatin in a similar configuration within the β-globin locus and LCR. Global analysis of EKLF-GATA1 and GATA1 ChIP-seq data sets also revealed a significant number of shared sites on the genomic scale.

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Heme and GATA1 coordinately regulate erythroid differentiation [expression]

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Project description:Naturally occurring mutations in the Î³-globin promoters can result in hereditary persistence of fetal hemoglobin (HPFH), a benign condition that ameliorates the severity of Î²-hemoglobinopathies through increased post-natal fetal hemoglobin (HbF) expression. Mutations in the Î³-globin promoters result in loss or de novo recruitment of transcription factors, yet the cis-regulatory elements involved in Î³-globin transcription in the context of HPFH are not clearly defined. We demonstrate that the -115 cluster of HPFH mutations require GATA1 binding to at -186 in cooperation with NF-Y at the proximal CCAAT box at -85 for Î³-globin expression. We show that multiple HPFH mutations increase HbF in an erythroid cell line and result in GATA1 binding at -186. Mutation of the -186 GATA motif in HPFH erythroid cell lines and erythroid-differentiated CD34+ cells resulted in loss of GATA1 binding and reduction in fetal hemoglobin. NF-Y ChIP-seq in HPFH erythroid cell lines demonstrated binding to the proximal CCAAT box at -85 was also found to be critical for HPFH-mediated Î³-globin expression. Together, the -186 GATA motif and -85 proximal CCAAT box function in an additive and independent manner. Our results reveal detailed evidence for common, positive acting cis-regulatory elements that may provide more general mechanisms for erythroid gene expression.

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HEXIM1 Overexpression Alters GATA1 Activity and Promotes Fetal Globin Expression

Project description:Erythropoiesis is a highly organized process whereby multipotent HSCs become committed to the erythroid linage and mature into enucleate erythrocytes. Recent work from our lab demonstrated that HEXIM1 is essential in the regulation of erythroid proliferation, viability and gene expression, and also promotes the expression of GATA1 target genes. New analyses of HEXIM1 overexpression (OE) in HUDEP2 cells revealed a significant increase of gamma globin production, with a higher proportion of cells expressing fetal hemoglobin. To gain insights into the mechanisms underlying the increased fetal globin expression, we performed CUT&RUN assays for Ser5 phosphorylated and total RNPII in HEXIM1 OE and control cells. Surprisingly, OE of HEXIM1 had only modest impacts on RNPII pausing, but instead lead to changes in the genes occupied by RNPII. Our results support a model where elevated HEXIM1 levels promote the pioneer activity of GATA1, and facilitate the expression of a fetal transcriptional program in adult cells in a pTEFb-dependent manner.

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