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DOT1L-mediated Murine Neuronal Differentiation associates with H3K79me2 Accumulation and preserves SOX2-Enhancer Accessibility

ABSTRACT: DOT1L-mediated Murine Neuronal Differentiation associates with H3K79me2 Accumulation and preserves SOX2-Enhancer Accessibility

PROVIDER: PRJNA558383 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11878619_1.fastq.gz	Fastqsanger.gz
	SRR11878619_2.fastq.gz	Fastqsanger.gz
	SRR11878620_1.fastq.gz	Fastqsanger.gz
	SRR11878620_2.fastq.gz	Fastqsanger.gz
	SRR11878621_1.fastq.gz	Fastqsanger.gz

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DOT1L-mediated Murine Neuronal Differentiation associates with H3K79me2 Accumulation and preserves SOX2-Enhancer Accessibility

Project description:To study whether acute inhibition of DOT1L induces global chromatin states alterations, we profile and compare the transcriptome, chromatin accessibility and epigenome (H3K4me3, H3K4me1, H3K27ac, H3K27me3, H3K36me3, H3K9me3, H3K79me2) of mESC and ES-derived NPC, treated with DMSO or EPZ5676.

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DOT1L-mediated murine neuronal differentiation associates with H3K79me2 accumulation and preserves SOX2-enhancer accessibility.

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DOT1L-mediated H3K79me2 directs B-cell repertoire establishment, marginal zone development and germinal center function

Project description:DOT1L is an epigenetic regulator that promotes gene expression by methylating lysine 79 on histone H3 and recruits transcription factors to gene targets. DOT1L is also an oncogenic driver in cancers that affect developing lymphocytes, yet how DOT1L activity regulates B-cell maturation remains poorly defined. Here, we use deep-sequencing and conditional knockout models to elucidate gene targets of H3K79me2, and the mechanistic contribution of DOT1L, during key stages of murine B-cell development. In the bone marrow, Dot1l was upregulated in pro B-cells. Deep-sequencing revealed that H3K79me2 accumulated during maturation. The genomic distribution of H3K79me2 peaks indicating that DOT1L regulates transcription and the cell cycle across different stages of B-cell development. As such, DOT1L was found to be essential for pre B-cell expansion, leading to a significant decrease in pre B-cells in the absence of DOT1L and a skewing of the B-cell receptor repertoire to favor proximal VH usage. In addition to the effective generation of a diverse B-cell pool, DOT1L was also required to establish the marginal zone (MZ) B-cell gene expression program. Attenuation of MZ B-cells and a bottlenecking at the pre-MZ B-cell stage in Dot1L-deficient mice correlated to H3K79me2 peaks at key MZ-regulatory genes such as Lfng and Dock10 in developing B cells. In contrast, Dot1l was re-expressed in germinal center (GC) B-cells post-immunization to deposit H3K79me2 at key GC B-cell gene loci during GC differentiation. Together, these data demonstrate a vital role for DOT1L during B cell lymphopoiesis, MZ B-cell generation and GC B-cell biology.

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Project description:Aberrant H3K79 dimethylation by DOT1L is a defining feature of MLL-rearranged (MLLr) acute myeloid leukemia (AML), but whether this modification influences alternative splicing remains unclear. Here, we performed H3K79me2 ChIP-seq and RNA-seq on primary samples from 24 MLLr AML patients, 4 wild-type MLL AML patients, and 4 healthy bone marrow donors. We found that a subset of exon skipping (SE) events was enriched at H3K79me2-occupied loci in MLLr samples. DOT1L inhibition with EPZ5676 led to broad changes in SE patterns, and many switched events showed concurrent reduction in local H3K79me2 signal. Pathway analysis of genes harboring these events revealed enrichment for RNA processing and splicing-related functions, with additional involvement of DNA repair and apoptosis-associated pathways. To identify potential mediators, we performed rapid immunoprecipitation mass spectrometry (RIME) in MV4-11 and MOLM-14 cells and detected SRSF2 and hnRNP family proteins in complex with DOT1L; these interactions were confirmed by co-immunoprecipitation. Combined inhibition of DOT1L and selected splicing factors reduced cell proliferation more effectively than single-agent treatment, both in MLLr cell lines and in xenograft models. These results indicate that H3K79me2 contributes to alternative splicing regulation through splicing factor recruitment in MLLr AML and provide a rationale for coordinated epigenetic–splicing therapeutic strategies.

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Project description:Histone modifications play a crucial role in regulating pulmonary branching morphogenesis, yet their specific contributions remain incompletely understood. Here, we demonstrate that H3K79me2 is broadly distributed throughout the airway epithelium in the early developmental stages of mouse embryonic lungs. Inhibition of H3K79me2 through EPZ5676, a DOT1L inhibitor, significantly enhanced branching morphogenesis in lung explant cultures. RNA-seq analysis revealed that EPZ5676 promotes epithelial cell differentiation and proliferation. Notably, in mesenchyme-free cultures, EPZ5676 alone did not influence epithelial morphogenesis but synergistically stimulated epithelial branching in the presence of FGF7. These findings identify H3K79me2 as a potential negative regulator of pulmonary branching morphogenesis and highlight the DOT1L inhibitor EPZ5676 as a promising epigenetic therapeutic target for promoting lung development and addressing pulmonary developmental disorders.

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Project description:We studied the role of the histone methyltransferase DOT1L in B cell development and differentiation. H3K79me2 ChIP-sequencing data was generated from sorted B cells. This was compared to RNA-sequencing data from WT and Dot1L KO mice in order to study the link between H3K79me2 and transcription.

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