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Molecular Dissection of Polycomb Group Protein-mediated Fetal Hemoglobin Repression

ABSTRACT: Molecular Dissection of Polycomb Group Protein-mediated Fetal Hemoglobin Repression

PROVIDER: PRJNA902776 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22324700_1.fastq.gz	Fastqsanger.gz
	SRR22324700_2.fastq.gz	Fastqsanger.gz
	SRR22324900_1.fastq.gz	Fastqsanger.gz
	SRR22324900_2.fastq.gz	Fastqsanger.gz
	SRR22324701_1.fastq.gz	Fastqsanger.gz

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Molecular Dissection of Polycomb Group Protein-mediated Fetal Hemoglobin Repression [RNA-seq]

Project description:Molecular Dissection of Polycomb Group Protein-mediated Fetal Hemoglobin Repression [RNA-seq]

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Molecular Dissection of Polycomb Group Protein-mediated Fetal Hemoglobin Repression [CUT&RUN]

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Molecular Dissection of Polycomb Group Protein-mediated Fetal Hemoglobin Repression [RNA-seq]

Project description:The fetal (HbF)-to-adult (HbA) hemoglobin switch is a paradigm for developmental gene expression control with relevance to sickle cell disease and beta-thalassemia. Polycomb repressive complex (PRC) proteins regulate this switch, and an inhibitor of the EED subunit of PRC2 entered clinical trials for fetal hemoglobin activation. Yet, how PcG complexes function in this process, their target genes and relevant subunit composition are unknown. Here, we identified the PRC1 subunit BMI1 as a novel HbF repressor. We uncovered LIN28B, IGF2BP1, and IGF2BP3 as direct BMI1 targets and demonstrate that they account for the BMI1 effects. BMI1 functions as part of the canonical PRC1 (cPRC1) subcomplex as revealed by the physical and functional dissection of BMI1 protein partners. Lastly, we demonstrate that BMI1/cPRC1 acts in concert with the PRC2 to repress HbF through the same target genes. Our study illuminates how PRC silences HbF, highlighting an epigenetic mechanism involved in hemoglobin switching.

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Direct Promoter Repression by BCL11A Controls the Fetal to Adult Hemoglobin Switch

Project description:Fetal hemoglobin (HbF) level is genetically controlled and modifies severity of adult hemoglobin (HbA) disorders. Common genetic variation affects expression of BCL11A, a critical regulator of HbF silencing. Current models suggest that BCL11A acts at a distance from the gamma-globin genes via long-distance chromosomal interactions. Here we use a functional cellular assay and protein-binding microarray to establish a requirement for a zinc-finger cluster of BCL11A for globin repression, and identify a preferred DNA recognition sequence (TGACCA). The motif is present in embryonic and fetal-expressed globin promoters, and duplicated in gamma-globin promoters, yet only the distal motif is mutated in alleles of individuals with hereditary persistence of hemoglobin. Using CUT&RUN to map protein binding sites, we detected BCL11A occupancy preferentially at the distal motif, and validated its absence in HbF-expressing, promoter-edited erythroid cells. Taken together, our findings reveal that direct gamma-globin gene promoter repression by BCL11A underlies hemoglobin switching.

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Direct Promoter Repression by BCL11A Controls the Fetal to Adult Hemoglobin Switch

Project description:Direct Promoter Repression by BCL11A Controls the Fetal to Adult Hemoglobin Switch

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Molecular Dissection of Polycomb Group Protein-mediated Fetal Hemoglobin Repression

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

2023-03-01 | GSE218233 | GEO

microRNA expression profiles of reticulocytes for hereditary persistence of fetal hemoglobin and β-thalssemia minor with high fetal hemoglobin.

Project description:We used microarrays to investigate differential microRNA (miRNA) expression in reticulocytes comparing reticulocytes from control individuals with normal fetal hemoglobin (HbF) level to hereditary persistence of fetal hemoglobin (HPFH) and β-thalssemia minor with high HbF, and try to find out some miRNAs associated with the mechanisms of HbF induction.

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The long noncoding RNA expression profiles of reticulocytes for hereditary persistence of fetal hemoglobin and β-thalssemia minor with high fetal hemoglobin.

Project description:To explore long noncoding RNA (lncRNA) expression and the biological functions of lncRNAs in fetal hemoglobin (HbF) induction, we surveyed lncRNA and mRNA expression profiles using circulating reticulocytes isolated from individuals with hereditary persistence of fetal hemoglobin (HPFH) and β-thalassaemia minor with high HbF.

2018-01-01 | GSE93971 | GEO

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