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

PROVIDER: PRJNA649591 | ENA |

REPOSITORIES: ENA

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

Project description: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.

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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.

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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.

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Project description:We studied the role of the histone methyltransferase DOT1L in B cell development and differentiation. Here we generated RNA-seq data naive B cells from (WT) MB1+/-;Dot1L+/+ and Dot1L KO (MB1+/-;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.

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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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Gene expression in LCMV-specific Blimp-1 deficient effector CD8+ T cells compared to wildtype effector CD8+ T cells

Project description:Antigen-specific effector CD8+ T cells deficient in Blimp-1 (Prdm1) do not acquire maximal effector functions, evade terminal differentiation, and more rapidly acquire some hallmark properties of memory CD8+ T cells. In this study, we compared the gene expression profiles of wildtype and Prdm1-/- LCMV-specific effector CD8+ T cells to better understand the molecular mechanisms underlying this striking phenotype. DNA microarray analysis was performed of DbGP33-41 and DbNP396-404 tetramer-positive effector CD8+ T cells FACS-sorted at day 8 post-LCMV infection from four independent samples of either Blimp-1 conditional knockout mice (CKO; Blimp-1flox/flox x GranzymeB-cre+) or wildtype (WT) littermate controls.

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Degree of Recruitment of DOT1L to MLL-AF9 Defines Level of H3K79 Di- and Tri-methylation on Target Genes and Transformation Potential

Project description:The MLL gene is a common target of chromosomal translocations found in human leukemia. MLL-fusion leukemias are consistently poor prognosis. One of the most common translocation partners is AF9 (a.k.a. MLLT3). MLL-AF9 recruits DOT1L, a histone 3 lysine 79 methyltransferase (H3K79me1/me2/me3), leading to aberrant gene transcription. We show that DOT1L has three AF9 binding sites, and present the NMR solution structure of a DOT1L-AF9 complex. We generated structure-guided point mutations with graded effects on recruitment of DOT1L to MLL-AF9. ChIP-Seq analyses of H3K79me2 and H3K79me3 show that graded reduction of the DOT1L interaction with MLL-AF9 results in selective losses in H3K79me2 and me3 marks at MLL-AF9 target genes. Furthermore, the degree of DOT1L recruitment defines the level of MLL-AF9 hematopoietic transformation. Hematopoietic progenitor cells isolated from mouse bone marrow were transduced with retrovirus expressing either wildtype MLL-AF9 (WT), mutants, MLL-AF9 (D544R) and MLL-AF9 (D546R). ChIP-Seq analyses were performed on these wildtype and mutant cells using H3K79me2 and H3K79me3 antibodies. 3 samples corresponding to ChIP-Seq with H3K79me2 antibody: 1) MLL-AF9 (WT) 2) MLL-AF9 (D544R) 3) MLL-AF9 (D546R) 3 Samples Corresponding to ChIP-Seq with H3K79me3 antibody: 4) MLL-AF9 (WT) 5) MLL-AF9 (D544R) 6) MLL-AF9 (D546R)

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Assesment of DOT1L direct targets via ChIP of H3K79me2 at E12.5 of mouse cortex

Project description:Cortical development is under control of transcriptional programs that are orchestrated by activation of key determinants such as transcription factors. But stable inheritance of temporo-spatial activity of factors influencing cell fate and regionalization in different layers is only partly understood. We report that chromatin methylation at H3K79 transmits cell fate and layering information from early to late progenitors. Activity of DOT1L, mediating H3K79 methylation, prevents premature cell cycle exit by increasing expression of genes regulating asymmetric cell division (Vangl2, Cenpj). Transcriptional programs characteristic for upper layer neurons are less active in Dot1l-deficient mice already at developmental stages that precede upper layer neuron generation. DOT1L activates expression of many key determinants such as Cux1, Cux2, Satb2 or Pou3f3. Additionally, DOT1L affects transcription of Sox family members, suggesting an evolutionary conserved mechanism. In part, DOT1L and H3K79me2 replace inactivating H3K9me3 at Sox family promoters and allow for transcriptional activation during neural differentiation.

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RNA expression in WT and Dot1L KO CD8 T cell subsets

Project description:RNA expression in WT and Dot1L KO CD8 T cell subsets

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