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

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

PROVIDER: PRJNA902781 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22324700_1.fastq.gz	Fastqsanger.gz
	SRR22324700_2.fastq.gz	Fastqsanger.gz
	SRR22324701_1.fastq.gz	Fastqsanger.gz
	SRR22324701_2.fastq.gz	Fastqsanger.gz
	SRR22324702_1.fastq.gz	Fastqsanger.gz

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Molecular Dissection of Polycomb Group Protein-mediated Fetal Hemoglobin Repression

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

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

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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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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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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CUT&RUN of erythroblasts upon perturbation of gamma-hemoglobin repressors (part II)

Project description:Through high throughput compound screening, we've identified compounds that induce the expression of fetal hemoglobin. This study contains CUT&RUN data of a novel target, WIZ.

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RNA-seq and CUT&RUN of erythroblasts upon perturbation of gamma-hemoglobin repressors

Project description:Through high throughput compound screening, we've identified compounds that induce the expression of fetal hemoglobin. This study contains RNA-seq and CUT&RUN data of a novel target, WIZ.

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Transcription factor competition at the γ-globin promoters controls hemoglobin switching [CUT&RUN]

Project description:BCL11A, the major regulator of HbF(α2γ2) level, represses γ-globin expression through direct promoter binding in adult erythroid cells in a switch to adult adult-type HbA (α2β2) production. Yet, the mechanism remains unclear. To uncover how BCL11A initiates repression, we used CRISPR/Cas9 and dCas9 screens to dissect the γ-globin promoters and identified an apparent activator element near the BCL11A binding region. Using CUT&RUN and base editing approaches, we demonstrate that this element, the proximal CCAAT box, is the binding site of transcription activator NF-Y. BCL11A competes with NF-Y binding through steric hindrance to initiate γ-globin repression, and the distance between the two motifs is critical for direct competition. Occupancy of NF-Y is rapidly established upon BCL11A depletion, and precedes γ-globin derepression and LCR-globin loop formation. Our findings reveal that the critical fetal-to-adult hemoglobin switch is initiated by the competition between transcription factors within a discrete region in the γ-globin promoters.

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Polycomb-mediated repression of paternal chromosomes maintains haploid dosage in diploid embryos of Marchantia [CUT&RUN]

Project description:Polycomb-mediated repression of paternal chromosomes maintains haploid dosage in diploid embryos of Marchantia [CUT&RUN]

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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