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Expression profiling of WT and Dot1L KO CD8 effector T cells and H3K79me2 occupancy in WT effector CD8 T cells

ABSTRACT: We studied the role of the histone methyltransferase DOT1L in T cell development and differentiation. We generated RNA-seq data from sorted CD8 effector T cells from WT (Lck-cre+/-) and Dot1L KO (Lck-cre+/-;Dot1Lfl/fl) mice infected with Listeria monocytogenes. This data was compared with H3K79me2 ChIP-seq data from the same T cell subset.

ORGANISM(S): Mus musculus

PROVIDER: GSE155406 | GEO | 2021/08/01

REPOSITORIES: GEO

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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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H3K79me2 and H3K4me3 in CD8 T cell subsets

Project description:We studied the role of the histone methyltransferase DOT1L in T cell development and differentiation. H3K79me2 and H3K4me3 ChIP-sequencing data was generated from sorted CD8 single positive thymocytes, naïve CD8 splenocytes and memory CD8 splenocytes. This was compared to RNA-sequencing data from WT and Dot1L KO mice in order to study the link between H3K79me2 and transcription.

2020-07-29 | GSE138908 | GEO

H3K79me2 Profiling Reveals DOT1L Regulated Splicing in MLL-rearranged AML [RNA-Seq]

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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H3K79me2 Profiling Reveals DOT1L Regulated Splicing in MLL-rearranged AML [ChIP-Seq]

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RNA expression in WT and Dot1L KO CD8 T cell subsets

Project description:We studied the role of the histone methyltransferase DOT1L in T cell development and differentiation. Here we generated RNA-seq data from sorted CD8 subpopulations from WT (Lcre+/-) and Dot1L KO (Lcre+/-;Dot1Lfl/fl) mice. This data was to define tissue specific expression signatures and it was compared with H3K79me2 ChIP-seq data from the same subsets.

2020-07-29 | GSE138910 | GEO

Expression profiling of WT and Dot1L KO CD8 effector T cells and H3K79me2 occupancy in WT effector CD8 T cells

Project description:Expression profiling of WT and Dot1L KO CD8 effector T cells and H3K79me2 occupancy in WT effector CD8 T cells

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DOT1L enhances BLM-induced pulmonary fibrosis by inducing endothelial-to-mesenchymal transition via H3K79me2 [ChIP-seq]

Project description:Endothelial-to-mesenchymal transition (EndoMT) have been reported to contribute to pulmonary fibrosis. Here, we showed that induction of EndoMT activated DOT1L expression and enhanced H3K79me2 level by TGFβ2 in human umbilical vein endothelial cells (HUVECs) in vitro. Using a bleomycin (BLM)-induced idiopathic pulmonary fibrosis (IPF) model, endothelial-lineage tracing reporter mice, and endothelial-specific Dot1L knockout mice, we confirmed that DOT1L mediates EndoMT and drives pulmonary fibrosis in vivo through H3K79 methylation. ChIP-seq revealed direct binding of SMAD2/3 to the DOT1L promoter and increased H3K79me2 deposition at fibrosis-related genes following TGFβ2 stimulation.

2026-04-01 | GSE299484 | GEO

DOT1L enhances BLM-induced pulmonary fibrosis by inducing endothelial-to-mesenchymal transition via H3K79me2 [ChIP-seq]

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DOT1L enhances BLM-induced pulmonary fibrosis by inducing endothelial-to-mesenchymal transition via H3K79me2 [RNA-seq]

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Inhibition of H3K79me2 by DOT1L inhibitor EPZ5676 promotes mouse embryonic lung branching morphogenesis via increasing epithelium proliferation

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.

2026-04-15 | GSE301374 | GEO

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