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CHD7 and Runx1 interaction provides a braking mechanism for hematopoietic differentiation [ATAC-seq]

ABSTRACT: Hematopoietic stem and progenitor cell (HSPC) formation and lineage differentiation involve gene expression programs orchestrated by transcription factors and epigenetic regulators. Knockdown of the chromatin remodeler chromodomain-helicase-DNA-binding protein 7 (CHD7) expanded phenotypic HSPCs, erythroid, and myeloid lineages in zebrafish and mouse embryos. CHD7 acts to suppress hematopoietic differentiation in a cell autonomous manner in the embryo and adult. CHD7 chromatin immunoprecipitation in human CD34+ and mouse HSPCs revealed enrichment of binding motifs for hematopoietic transcription factors including Runx1 and GATA factors, and decreased Runx1 occupancy correlated with loss of CHD7 occupancy. CHD7 physically interacts with Runx1 and suppresses Runx1-induced expansion of HSPCs during development, providing both physical and genetic evidence for the Runx1-CHD7 interaction. CHD7 modulates Runx1 activity to provide proper timing and function of HSPCs as they emerge during hematopoietic development or mature in adults, representing a distinct and evolutionarily conserved control mechanism to ensure accurate hematopoietic lineage differentiation.

ORGANISM(S): Mus musculus

PROVIDER: GSE130280 | GEO | 2023/01/01

REPOSITORIES: GEO

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CHD7 and Runx1 interaction provides a braking mechanism for hematopoietic differentiation [RNA-seq]

Project description:Hematopoietic stem and progenitor cell (HSPC) formation and lineage differentiation involve gene expression programs orchestrated by transcription factors and epigenetic regulators. Knockdown of the chromatin remodeler chromodomain-helicase-DNA-binding protein 7 (CHD7) expanded phenotypic HSPCs, erythroid, and myeloid lineages in zebrafish and mouse embryos. CHD7 acts to suppress hematopoietic differentiation in a cell autonomous manner in the embryo and adult. CHD7 chromatin immunoprecipitation in human CD34+ and mouse HSPCs revealed enrichment of binding motifs for hematopoietic transcription factors including Runx1 and GATA factors, and decreased Runx1 occupancy correlated with loss of CHD7 occupancy. CHD7 physically interacts with Runx1 and suppresses Runx1-induced expansion of HSPCs during development, providing both physical and genetic evidence for the Runx1-CHD7 interaction. CHD7 modulates Runx1 activity to provide proper timing and function of HSPCs as they emerge during hematopoietic development or mature in adults, representing a distinct and evolutionarily conserved control mechanism to ensure accurate hematopoietic lineage differentiation.

2023-01-01 | GSE84128 | GEO

CHD7 and Runx1 interaction provides a braking mechanism for hematopoietic differentiation [G1ER ChIP-seq]

2023-01-01 | GSE84129 | GEO

CHD7 and Runx1 interaction provides a braking mechanism for hematopoietic differentiation [CD34 ChIP-seq]

2023-12-01 | GSE84130 | GEO

CHD7 and Runx1 interaction provides a braking mechanism for hematopoietic differentiation

Project description:Hematopoietic stem and progenitor cell (HSPC) formation and lineage differentiation involve gene expression programs orchestrated by transcription factors and epigenetic regulators. Knockdown of the chromatin remodeler chromodomain-helicase-DNA-binding protein 7 (CHD7) expanded phenotypic HSPCs, erythroid, and myeloid lineages in zebrafish and mouse embryos. CHD7 acts to suppress hematopoietic differentiation in a cell autonomous manner in the embryo and adult. We performed ChIP sequencing to determine the genomic localization of CHD7 in human CD34+ and mouse HSPCs, revealing enrichment of binding motifs for hematopoietic transcription factors including Runx1 and GATA factors. CHD7 occupied regions are transcriptionally active and are near genes with hematopoietic function. Decreased Runx1 occupancy correlated with loss of CHD7 occupancy. Together, the physical and genetic interaction data support a model in which CHD7 interacts with and modulates Runx1 activity to provide proper timing and function of HSPCs as they emerge during hematopoietic development or mature in adults. This represents a distinct and evolutionarily conserved control mechanism to ensure accurate hematopoietic lineage differentiation.

2019-07-27 | GSE83956 | GEO

Expression Profile of CHD7-Deficient Murine Long-term Hematopoietic Stem Cells

2018-07-01 | GSE84136 | GEO

Expression analysis of Chd7 in mouse hematopoietic stem and progenitor cells [microarray]

Project description:Hematopoietic stem and progenitor cell (HSPC) formation and lineage differentiation involve gene expression programs orchestrated by transcription factors and epigenetic regulators. Knockdown of the chromatin remodeler chromodomain-helicase-DNA-binding protein 7 (CHD7) expanded phenotypic HSPCs, erythroid, and myeloid lineages in zebrafish and mouse embryos. CHD7 acts to suppress hematopoietic differentiation in a cell autonomous manner in the embryo and adult. We performed gene expression analysis to determine the expression of chd7 in adult sorted HSPC populations. Loss of Chd7 in long term hematopoietic stem cells (LT-HSCs) results in upregulation of genes that function in hematopoietic system development and function. Genes representative of each blood lineage including erythroid, myeloid, and lymphoid were upregulated, suggesting that Chd7 deficiency results in LT-HSCs that are more primed for multilineage differentiation. Together with the physical and genetic interaction, the data support a model in which CHD7 interacts with and modulates Runx1 activity to provide proper timing and function of HSPCs as they emerge during hematopoietic development or mature in adults. This represents a distinct and evolutionarily conserved control mechanism to ensure accurate hematopoietic lineage differentiation. We used microarrays to detail the expression of Chd7 in adult sorted HSPC populations.

2023-01-01 | GSE84127 | GEO

CHD7 and Runx1 interaction provides a braking mechanism for hematopoietic differentiation

Project description:CHD7 and Runx1 interaction provides a braking mechanism for hematopoietic differentiation

| PRJNA541162 | ENA

CHD7 and Runx1 interaction provides a braking mechanism for hematopoietic differentiation

Project description:We investigated the transcriptional consequences of Chd7 and Runx1 loss in 416B cells, a myeloid progenitor cell line. We engineered the cell line to express Cas9 protein and targeted endogenous Chd7 and Runx1 loci with sgRNAs introduced with lentiviral constructs. We read out the transcriptomes of control and perturbed cells using RNA-Seq following an established SMART-Seq2 protocol (Picelli et al. 2014).

2022-04-26 | GSE130719 | GEO

Gene regulation in hematopoietic cells by Pcgf1 in a Runx1 null background

Project description:The transcription factor Runx1 is essential for the establishment of definitive hematopoiesis during embryonic development. In adult blood homeostasis, Runx1 plays a pivotal role in the maturation of lymphocytes and megakaryocytes. Furthermore, Runx1 is required for the regulation of hematopoietic stem and progenitor cell (HSPC) pools. However, how Runx1 orchestrates self-renewal and lineage choices in combination with other factors is not well understood. Here we describe a genome-scale RNAi screen to detect genes that cooperate with Runx1 in regulating HSPCs. We identify the polycomb group protein Pcgf1 as an epigenetic regulator involved in hematopoietic cell differentiation. We show that simultaneous depletion of Runx1 and Pcgf1 allows sustained self-renewal while blocking differentiation of HSPCs in vitro. We find an upregulation of HoxA cluster genes upon Pcgf1 knockdown that possibly accounts for the increase in self-renewal. Further, our data suggest that cells lacking both Runx1 and Pcgf1 are blocked at an early progenitor stage, indicating that a concerted action of the transcription factor Runx1 together with the epigenetic repressor Pcgf1 is necessary for terminal differentiation. Thus, our work discovers a genetic link between transcriptional and epigenetic regulation that is required for hematopoietic differentiation. Hematopoietic stem and precursor cells freshly isolated from mice were transduced with an shRNA targeting Pcgf1 or a control shRNA. Cells were selected with puromycin for 36 h before total mRNA was isolated.

2012-06-17 | E-GEOD-33280 | biostudies-arrayexpress

Chromatin Remodeler CHD7 mutated in CHARGE Syndrome Interacts with Sox10 to Regulate Timing of CNS Myelination and Remyelination [ChIP-seq]

Project description:Mutations in CHD7, encoding ATP-dependent chromodomain-helicase-DNA-binding protein 7, in CHARGE syndrome leads to multiple congenital anomalies including growth retardation, craniofacial malformations and neurological dysfunction. Currently, mechanisms underlying the CNS phenotypes remain poorly understood. Here, we show that Chd7 is a direct transcriptional target of oligodendrogenesis-promoting factors Olig2 and Brg1 and required for proper timing of CNS myelination and remyelination. Genome-occupancy analyses coupled with transcriptome profiling reveal that Chd7 cooperates with Sox10 to target the enhancers of key myelinogenic genes, and identify novel Chd7 target. Examination of Chd7 and Sox10 genomewide occupancy in differentiating oligodendrocytes

2016-02-29 | E-GEOD-72725 | biostudies-arrayexpress

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