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TET2 regulates osteoclast differentiation by interacting with RUNX1 and maintaining genomic 5-hydroxymethylcytosine

ABSTRACT: TET2 regulates osteoclast differentiation by interacting with RUNX1 and maintaining genomic 5-hydroxymethylcytosine

PROVIDER: PRJNA413945 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6159180_1.fastq.gz	Fastqsanger.gz
	SRR6159180_2.fastq.gz	Fastqsanger.gz
	SRR6159181_1.fastq.gz	Fastqsanger.gz
	SRR6159181_2.fastq.gz	Fastqsanger.gz
	SRR6159182_1.fastq.gz	Fastqsanger.gz

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Tet2 Regulates Osteoclast Differentiation by Interacting with Runx1 and Maintaining Genomic 5-Hydroxymethylcytosine (5hmC).

Project description:As a dioxygenase, Ten-Eleven Translocation 2 (TET2) catalyzes subsequent steps of 5-methylcytosine (5mC) oxidation. TET2 plays a critical role in the self-renewal, proliferation, and differentiation of hematopoietic stem cells, but its impact on mature hematopoietic cells is not well-characterized. Here we show that Tet2 plays an essential role in osteoclastogenesis. Deletion of Tet2 impairs the differentiation of osteoclast precursor cells (macrophages) and their maturation into bone-resorbing osteoclasts in vitro. Furthermore, Tet2-/- mice exhibit mild osteopetrosis, accompanied by decreased number of osteoclasts in vivo. Tet2 loss in macrophages results in the altered expression of a set of genes implicated in osteoclast differentiation, such as Cebpa, Mafb, and Nfkbiz. Tet2 deletion also leads to a genome-wide alteration in the level of 5-hydroxymethylcytosine (5hmC) and altered expression of a specific subset of macrophage genes associated with osteoclast differentiation. Furthermore, Tet2 interacts with Runx1 and negatively modulates its transcriptional activity. Our studies demonstrate a novel molecular mechanism controlling osteoclast differentiation and function by Tet2, that is, through interactions with Runx1 and the maintenance of genomic 5hmC. Targeting Tet2 and its pathway could be a potential therapeutic strategy for the prevention and treatment of abnormal bone mass caused by the deregulation of osteoclast activities.

| S-EPMC6076382 | biostudies-literature

TET2 regulates osteoclast differentiation by interacting with RUNX1 and maintaining genomic 5-hydroxymethylcytosine

Project description:In this study we show that Tet2 helps regulate the differentiation of macrophages to osteoclases

2018-05-01 | GSE104828 | GEO

Transcriptome-wide survey of Runx1-interacting RNAs by RNA immunoprecipitation sequencing

Project description:Runt-related transcription factor 1 (RUNX1) plays critical roles in hematopoiesis including myeloid development. Runx1 binds Runt consensus motifs at promoters and regulatory elements of its target genes. Interestingly, several Runx1-binding RNA aptamers have been successfully developed. Additionally, mounting evidences suggest that transcription factors are capable of binding to RNAs. In this study, we performed a transcriptome-wide screen for Runx1-interacting RNAs in living cells using fRIP-Seq. Anti-Runx1 antibody was used to capture Runx1 in the monocytic cell line THP-1. RNAs co-immunoprecipitated with Runx1 were sequenced by paired-end massively parallel sequencing and analyzed by HOMER peak calling and annotation algorithms. By doing so, we identified a repertoire of RNAs interacting with Runx1. We further investigate functional role of these interactions in Runx1-mediated transcription regulation.

2021-10-27 | GSE140459 | GEO

Transcriptome-wide survey of Runx1-interacting RNAs by RNA immunoprecipitation sequencing

Project description:Transcriptome-wide survey of Runx1-interacting RNAs by RNA immunoprecipitation sequencing

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RUNX1 is a key target gene in t(4;11) leukemias and contributes to gene activation by interacting with the AF4-MLL complex

Project description:The Mixed Lineage Leukemia 1 protein (MLL1) is an important epigenetic regulator required for the maintenance of gene activation during development. MLL1 chromosome translocations produce novel fusion proteins that cause aggressive leukemias in humans. Individual MLL1 fusion proteins have distinct leukemic phenotypes even when expressed in the same cell type, but how this distinction is delineated on a molecular level is poorly understood. Here we highlight a unique molecular mechanism whereby MLL-AF4 specifically activates the RUNX1 gene and the RUNX1 protein interacts with the product of the reciprocal AF4-MLL translocation. These results support a mechanism of leukemic growth whereby two oncogenic fusion proteins cooperate by activating a target gene and then interacting directly with its downstream product ChIP-seq using RUNX1 antibody in SEM cells

2013-01-31 | E-GEOD-42075 | biostudies-arrayexpress

Sexually Dimorphic Increases in Bone Mass Following Tissue-specific Overexpression of Runx1 in Osteoclast Precursors

Project description:We investigated the skeletal effects of conditional overexpression of Runx1 in preosteoclasts by crossing novel Runx1 gain-of-function mice (Rosa26-LSL-Runx1) with LysM-Cre transgenic mice.

2022-10-24 | GSE216312 | GEO

Sexually Dimorphic Increases in Bone Mass Following Tissue-specific Overexpression of Runx1 in Osteoclast Precursors

Project description:Sexually Dimorphic Increases in Bone Mass Following Tissue-specific Overexpression of Runx1 in Osteoclast Precursors

| PRJNA892966 | ENA

Genome Wide Chromatin Mapping of H3K27me3 and H3K4me3 histone modifications in wild type and ASXL1-/- Osteoclast

Project description:We report a novel role of ASXL1 protein in altering epigentic profile of osteoclast. ASXL1 is an ETP protein that bind to polycomb repressive complex. We asked if ASXL1 regulates osteoclast differentiation by maintaining balance between positive and negative epigenetic regulators. To address this question, we performed ChIP-seq using H3K27me3 and H3K4me3 antbody in day2 osteoclast. Our data reveals that there was a global loss of H3K27me3 in ASXl1-/- osteoclast which includes loss of this repressive methylation of NFATc1 promoter, which is a master regulator of osteoclastogenesis.

2019-03-14 | GSE111852 | GEO

5-hydroxymethylcytosine poises expression of genes involved in hematopoietic differentiation

Project description:Epigenetic processes regulate hematopoietic stem cell homeostasis. The recent discovery of 5-hydroxymethylcytosine (5hmC) provides new insights into the epigenetic regulation of gene expression during development. We used reduced representation of 5-hydroxymethylcytosine profiling (RRHP) to characterize the genome-wide distribution of 5hmC in human CD34+ hematopoietic stem/progenitor cells, lymphocytes, monocytes and granulocytes. We show that 5hmC levels decrease during cell differentiation and that 5hmC is associated with H3K4me1 and H3K27ac histone modifications, indicative of active enhancers. In CD34+ cells, the presence of 5hmC at presumed active enhancers correlates with increased binding of RUNX1 and FLI1, two transcription factors essential for hematopoiesis. Moreover, in progenitor cells, 5hmC poises the expression of transcription factors regulating hematopoietic lineage commitment, such as RUNX1, FOXO1 and C/EBP-alpha. Our study provides the first comprehensive genome-wide overview of 5hmC distribution in human hematopoietic cells and of its potential role in transcriptional network regulation during hematopoiesis.

2016-06-02 | GSE69905 | GEO

RUNX1 is a key target gene in t(4;11) leukemias and contributes to gene activation by interacting with the AF4-MLL complex

2013-01-31 | GSE42075 | GEO