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

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

PROVIDER: PRJNA1215426 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32117946_1.fastq.gz	Fastqsanger.gz
	SRR32117946_2.fastq.gz	Fastqsanger.gz
	SRR32117947_1.fastq.gz	Fastqsanger.gz
	SRR32117947_2.fastq.gz	Fastqsanger.gz
	SRR32117948_1.fastq.gz	Fastqsanger.gz

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

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 | GSE287996 | GEO

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

2025-02-17 | GSE276903 | GEO

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

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

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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]

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

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

| PRJNA1159372 | ENA

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

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

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The strand-biased mitochondrial DNA methylome and its regulation by DNMT3A

Project description:The strand-biased mitochondrial DNA methylome and its regulation by DNMT3A

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The strand-biased mitochondrial DNA methylome and its regulation by DNMT3A [HEK293T_MeDIP]

Project description:How individual genes are regulated from a mitochondrial polycistronic transcript to have variable expression remains an enigma. Here, through bisulfite sequencing and strand-specific mapping, we show mitochondrial genomes in human and other animals were strongly biased to light (L)-strand non-CpG methylation with conserved peak loci preferentially located at gene-gene boundaries, which was also independently validated by MeDIP and FspEI digestion. Such mtDNA methylation patterns are conserved across different species and developmental stages, but display dynamic local or global changes during development and aging. Knockout of DNMT3A alone perturbed mtDNA regional methylation patterns, but not global levels, and altered mitochondrial gene expression, copy number, and oxygen respiration. Overexpression of DNMT3A strongly increased mtDNA methylation and strand bias. Overall, methylation at gene body and boundaries was negatively associated with mitochondrial transcript abundance and also polycistronic transcript processing. Furthermore, HPLC-MS confirmed the methylation signals on mitochondria DNA. Together, these data provide high-resolution mtDNA methylation maps that revealed a strand specific non-CpG methylation, its dynamic regulation and its impact on the polycistronic mitochondrial transcript processing. Through bisulfite sequencing and strand-specific mapping, we show mitochondrial genomes in human and other animals were strongly biased to light (L)-strand non-CpG methylation with conserved peak loci preferentially located at gene-gene boundaries, which was also independently validated by MeDIP and FspEI digestion.

2019-08-22 | GSE133958 | GEO

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.

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