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Genome-wide maps of H3K27ac in HDAC3 knockout bone marrow pDCs compared with control pDCs

ABSTRACT: Genome-wide maps of H3K27ac in HDAC3 knockout bone marrow pDCs compared with control pDCs

PROVIDER: PRJNA809374 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18100473_1.fastq.gz	Fastqsanger.gz
	SRR18100473_2.fastq.gz	Fastqsanger.gz
	SRR18100474_1.fastq.gz	Fastqsanger.gz
	SRR18100474_2.fastq.gz	Fastqsanger.gz
	SRR18100475_1.fastq.gz	Fastqsanger.gz

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Genome-wide maps of H3K27ac in HDAC3 knockout bone marrow pDCs compared with control pDCs

Project description:Hdac3 is highly expressed in pDCs, and its deficiency led to substantially impaired development of pDCs, but not cDCs in bone marrow (BM) and spleen. Meanwhile,further investigation demonstrated that HDAC3 was required for the differentiation of pDC from progenitors at different differentiation stages in vitro. Cut & Tag analysis of H3K27ac level in HDAC3 deficient bone marrow pDCs compared with control pDCs, showed that H3K27ac level significantly increased on cDC related genes with PU.1 binding sites in HDAC3 knockout pDCs.

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Next Generation Sequencing of transcriptomes to reveal the role of HDAC3 in regulating the development of LMPP and CD115- CDP and bone marrow pDCs

Project description:Hdac3 is highly expressed in pDCs, and its deficiency led to substantially impaired development of pDCs, but not cDCs in bone marrow (BM) and spleen. Meanwhile, the hematopoietic progenitors with DC differentiation potential, including CMP, CLP and CD115+ CDP were significantly decreased. Although the number of HSC and CD115− CDP were increased, their differentiation potential toward pDCs were abolished. Further investigation demonstrated that HDAC3 was required for the differentiation of pDC from progenitors at different differentiation stages.

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Project description:Histone deacetylase inhibitors are efficacious epigenetic-based therapies for some cancers and neurological disorders; however, these drugs inhibit multiple Hdacs and have detrimental effects on the pre- and post-natal skeleton. To better understand how Hdac inhibitors affect the skeleton, we focused on understanding the role of one of their targets, Hdac3, in endochondral bone formation by deleting it in immature murine chondrocyte micro masses with Adeno-Cre. Hdac3-deficient chondrocytes expressed higher levels of pro-inflammatory and matrix degrading genes (e.g., Il-6, Mmp3, Mmp13, Saa3) and lower levels of genes related to the extracellular matrix production, bone development and ossification (e.g., Acan, Col2a1, Ihh, Col10a1). Histone acetylation was increased in and around genes with elevated expression. This SuperSeries is composed of the SubSeries listed below. High Throughput RNA sequencing and Chromatin immunopreciptation sequencing experiments were performed in chondrocyte cultures. Differential analysis was conducted on ChIP-seq and RNA-seq data to identify H3K27Ac profiles for up and down-regulated genes in Hdac3-deficient murine chondrocytes. mm10 was used as reference genome. Refer to individual Series

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Project description:Determine the effects of Hdac3 deletion on H3K27ac profiles in murine chondrocytes

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