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DNMT3A regulates megakaryocyte-biased hematopoietic stem cell fate decisions [EMseq]

ABSTRACT: DNMT3A regulates megakaryocyte-biased hematopoietic stem cell fate decisions [EMseq]

PROVIDER: PRJNA1159372 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30623370_1.fastq.gz	Fastqsanger.gz
	SRR30623370_2.fastq.gz	Fastqsanger.gz
	SRR30623371_1.fastq.gz	Fastqsanger.gz
	SRR30623371_2.fastq.gz	Fastqsanger.gz
	SRR30623372_1.fastq.gz	Fastqsanger.gz

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DNMT3A regulates megakaryocyte-biased hematopoietic stem cell fate decisions [RNASeq]

Project description:DNMT3A regulates megakaryocyte-biased hematopoietic stem cell fate decisions [RNASeq]

| PRJNA1159369 | ENA

DNMT3A regulates megakaryocyte-biased hematopoietic stem cell fate decisions [RNASeq]

Project description:Hematopoietic stem cells (HSCs) are defined by their capacity to regenerate all main components of the peripheral blood, but individual HSCs exhibit a range of preferences for generating downstream cell types. Their propensities are thought to be epigenetically encoded, but no differential regulatory mechanisms have been identified. Here, we considered whether DNA methyltransferase 3A (DNMT3A) has a role in determining the differentiation choice of HSCs. We find that the most primitive megakaryocyte-biased HSCs depend most on DNMT3A for efficient hematopoietic regeneration, particularly of the lymphoid lineages. Reduced DNMT3A amplifies the biased HSC behavior. DNMT3A also regulates megakaryocyte and platelet output in part through DNA methylation at key megakaryocyte lineage loci. Together, our findings establish the role of epigenetic regulation in the fate of megakaryocyte-biased HSCs and their downstream progeny and suggest that the outcomes of DNMT3A-mutant clonal hematopoiesis and malignancies might vary depending on the identity of the HSC that acquires the mutation.

2025-02-17 | GSE276901 | GEO

DNMT3A regulates megakaryocyte-biased hematopoietic stem cell fate decisions [EMseq]

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DNMT3A regulates megakaryocyte-biased hematopoietic stem cell fate decisions [EM-Seq]

2025-02-17 | GSE287996 | GEO

DNMT3A regulates megakaryocyte-biased hematopoietic stem cell fate decisions [RNA-Seq]

2025-02-17 | GSE287995 | GEO

DNMT3A regulates megakaryocyte-biased hematopoietic stem cell fate decisions [RNA-Seq]

Project description:DNMT3A regulates megakaryocyte-biased hematopoietic stem cell fate decisions [RNA-Seq]

| PRJNA1215424 | ENA

DNMT3A regulates megakaryocyte-biased hematopoietic stem cell fate decisions [EM-Seq]

Project description:DNMT3A regulates megakaryocyte-biased hematopoietic stem cell fate decisions [EM-Seq]

| PRJNA1215426 | ENA

De novo DNA methylation by DNA Methyltransferase 3a controls early effector CD8+ T cell fate decisions following activation

Project description:DNMT3a is a de novo DNA methyltransferase expressed robustly after T cell activation that regulates plasticity of CD4+ T cell cytokine expression. Here we show that DNMT3a is critical for directing early CD8+ T cell effector and memory fate decisions. While effector function of DNMT3a knockout T cells is normal, they develop more memory precursor and fewer terminal effector cells in a T cell intrinsic manner compared to wild-type animals. Rather than increasing plasticity of differentiated effector CD8+ T cells, loss of DNMT3a biases differentiation of early effector cells into memory precursor cells. This is attributed in part to ineffective repression of Tcf1 expression in knockout T cells, as DNMT3a localizes to the Tcf7 promoter and catalyzes its de novo methylation in early effector WT CD8+ T cells. This data identifies DNMT3a as a crucial regulator of CD8+ early effector cell differentiation and effector versus memory fate decisions. Examination of global genomic DNA methylation by MBD-seq in naÃ¯ve CD8 T cells and CD8 T cells 8 days post Vaccinia-Ova infection, comparing OT1 TCR-Tg CD8 T cells isolated from WT and T cell conditional DNMT3a KO mice.

2016-08-20 | E-GEOD-85823 | biostudies-arrayexpress

De novo DNA methylation by DNA Methyltransferase 3a controls early effector CD8+ T cell fate decisions following activation

2016-08-20 | GSE85823 | GEO

The endogenous antigen-specific CD8+ T cell repertoire is composed of unbiased and biased clonotypes with differential fate commitment.

Project description:Generating balanced populations of CD8+ effector and memory T cells is necessary for immediate and durable immunity to infections and cancer. Yet, a definitive understanding of how a diverse CD8+ T cell repertoire differentiates remains unclear. We identified several hundred TCR clonotypes that constitute the polyclonal response against a single antigen and found that a majority of TCR clonotypes were highly biased towards memory or effector fate. TCR-intrinsic biases were not stochastic and were dominant over environmental cues. Differential gene expression analysis of memory- or effector-biased TCR clonotypes showed bifurcation of differential fates at the early effector stage. Additionally, phylogenetic analysis revealed that memory-biased clonotypes retain their fate preferences in subclonal populations but effector-biased subclones can switch to memory fate. Our study highlights that the polyclonal CD8+ T cell response is a composite of unbiased and biased clonotypes with varying capacity to incorporate environmental cues in their cell fate decisions.

2025-02-27 | GSE241403 | GEO

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