Gene regulation by PCGF1 in hematopoietic progenitor cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA699535 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13631500_1.fastq.gz | Fastqsanger.gz | |||
| SRR13631500_2.fastq.gz | Fastqsanger.gz | |||
| SRR13631501.fastq.gz | Fastqsanger.gz | |||
| SRR13631502.fastq.gz | Fastqsanger.gz | |||
| SRR13631497_1.fastq.gz | Fastqsanger.gz |
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Project description:Gene regulation by PCGF1 in hematopoietic progenitor cells [ChIP, MNaseSeq]
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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
Project description:Polycomb proteins are epigenetic regulators important for cell fate decision and maintenance. Here we show that PCGF1, one of components of Polycomb repressive complex (PRC) 1 is important for the differentiation of hematopoietic stem/progenitor cells (HSPCs) towards lymphoid lineage. The deletion of Pcgf1 in HSPCs lead to severe defects in B cell development with an expansion of myeloid progenitors. The blockade of B cell differentiation occurred at the lymphoid-primed multipotent progenitor (LMPP) stage. Chromatin immunoprecipitation followed by DNA sequencing analysis of normal LMPP-like cells demonstrated that PCGF1 colocalized with RING1A/B and PRC2. Upon deletion of Pcgf1, we found dramatic decline of H3K27me3 levels, resulting in de-repression of target genes. Strikingly, the occupancy of RING1A/B, PRC2 and monoubiquitination of histone H2A at lysin 119 on the target loci was not affected. These results demonstrate that the PCGF1 safeguards the immune system development by directly regulating the PRC2-mediated H3K27me3 levels.
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Project description:Gene regulation by PCGF1 in hematopoietic progenitor cells [ChIP and MNaseSeq]
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Project description:Polycomb proteins are epigenetic regulators important for cell fate decision and maintenance. Here we show that PCGF1, one of components of Polycomb repressive complex (PRC) 1 is important for the differentiation of hematopoietic stem/progenitor cells (HSPCs) towards lymphoid lineage. The deletion of Pcgf1 in HSPCs lead to severe defects in B cell development with an expansion of myeloid progenitors. The blockade of B cell differentiation occurred at the lymphoid-primed multipotent progenitor (LMPP) stage. Chromatin immunoprecipitation followed by DNA sequencing analysis of normal LMPP-like cells demonstrated that PCGF1 colocalized with RING1A/B and PRC2. Upon deletion of Pcgf1, we found dramatic decline of H3K27me3 levels, resulting in de-repression of target genes. Strikingly, the occupancy of RING1A/B, PRC2 and monoubiquitination of histone H2A at lysin 119 on the target loci was not affected. These results demonstrate that the PCGF1 safeguards the immune system development by directly regulating the PRC2-mediated H3K27me3 levels.
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Project description:Polycomb proteins are epigenetic regulators important for cell fate decision and maintenance. Here we show that PCGF1, one of components of Polycomb repressive complex (PRC) 1 is important for the differentiation of hematopoietic stem/progenitor cells (HSPCs) towards lymphoid lineage. The deletion of Pcgf1 in HSPCs lead to severe defects in B cell development with an expansion of myeloid progenitors. The blockade of B cell differentiation occurred at the lymphoid-primed multipotent progenitor (LMPP) stage. Chromatin immunoprecipitation followed by DNA sequencing analysis of normal LMPP-like cells demonstrated that PCGF1 colocalized with RING1A/B and PRC2. Upon deletion of Pcgf1, we found dramatic decline of H3K27me3 levels, resulting in de-repression of target genes. Strikingly, the occupancy of RING1A/B, PRC2 and monoubiquitination of histone H2A at lysin 119 on the target loci was not affected. These results demonstrate that the PCGF1 safeguards the immune system development by directly regulating the PRC2-mediated H3K27me3 levels.
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