CHD7 and Runx1 interaction provides a braking mechanism for hematopoietic differentiation
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ABSTRACT:
PROVIDER: PRJNA328122 | ENA |
REPOSITORIES: ENA
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Project description:CHD7 and Runx1 interaction provides a braking mechanism for hematopoietic differentiation
| PRJNA541162 | ENA
Project description:CHD7 and Runx1 interaction provides a braking mechanism for hematopoietic differentiation [ATAC-seq]
| PRJNA534517 | ENA
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 | GSE130280 | GEO
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
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
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.
2023-12-01 | GSE84130 | GEO
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 | GSE84129 | GEO
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
Project description:CHD7 and Runx1 interaction provides a braking mechanism for hematopoietic differentiation
| PRJNA328994 | ENA
Project description:Hematopoietic stem and progenitor cell (HSPC) formation and lineage differentiation involve gene expression programs orchestrated by transcription factors and epigenetic regulators. Genetic disruption 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. Binding motifs for RUNX and other hematopoietic transcription factors are enriched at sites occupied by CHD7, and decreased RUNX1 occupancy correlated with loss of CHD7 localization. CHD7 physically interacts with RUNX1 and suppresses RUNX1-induced expansion of HSPCs during development through modulation of RUNX1 activity. Consequently, the RUNX1:CHD7 axis provides 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.
| S-EPMC7519295 | biostudies-literature