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RNA-sequencing of Dot1L-deficient B cell subsets

ABSTRACT: RNA-sequencing of Dot1L-deficient B cell subsets

PROVIDER: PRJNA575736 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10227679.fastq.gz	Fastqsanger.gz
	SRR10227680.fastq.gz	Fastqsanger.gz
	SRR10227681.fastq.gz	Fastqsanger.gz
	SRR10227682.fastq.gz	Fastqsanger.gz
	SRR10227683.fastq.gz	Fastqsanger.gz

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RNA-sequencing of Dot1L-deficient B cell subsets

Project description:We assessed gene expression differences in B cells from mice in which Dot1L is conditionally deleted in mature B cells

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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:Genome-wide mapping of H3K9me2 in DOT1L-deficient worms.

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Transcriptional profiling of naïve and in vitro activated B cells from WT and DOT1L KO mice

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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Global gene expression analysis of Dot1l-deficient and control intestinal villus cells in mouse

Project description:Methylation of H3K79 is associated with chromatin at expressed genes, though it is unclear if this histone modification is required for transcription of all genes. Recent studies suggest that Wnt-responsive genes depend particularly on H3K79 methylation, which is catalyzed by the methyltransferase DOT1L. Human leukemias carrying MLL gene rearrangements show DOT1L-mediated H3K79 methylation and aberrant expression of leukemogenic genes. DOT1L inhibitors reverse these effects but their clinical use is potentially limited by toxicity in Wnt-dependent tissues such as intestinal epithelium. Genome-wide positioning of the H3K79me2 mark in Lgr5+ mouse intestinal stem cells and mature intestinal villus epithelium correlated with mRNA expression levels but not with Wnt-responsive genes per se. Selective Dot1l disruption in Lgr5+ stem cells or in all intestinal epithelial cells eliminated H3K79me2 from the respective compartments, allowing genetic evaluation of DOT1L requirements. Absence of methylated H3K79 did not impair health, intestinal homeostasis or expression of Wnt target genes in crypt epithelium for up to 4 months, despite increased crypt cell apoptosis. Global transcript profiles in Dot1l-null cells were barely altered. Thus, H3K79 methylation is not essential for transcription of Wnt-responsive or other intestinal genes and intestinal toxicity is not imperative when DOT1L is rendered inactive in vivo. Examination of differential gene expression between Dot1l control (Dot1 f/f) and Dot1l mutant (Villin-Cre, Dot1l f/f) villus cells.

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The Histone Methyltransferases MLL1 and DOT1L Cooperate with Meningioma-1 to Induce AML [Mouse Dot1l ko RNA-seq]

Project description:Purpose: To characterize transcriptional changes associated with homozygous inactivation of Dot1l or Mll1 in MN1 driven AML Methods: We sequenced mRNA from murine LSK-cells transformed using forced expression of MN1 (MSCV-MN1-IRES-GFP), and transduced with Cre-vector to inactivate either Dot1l or Mll1. Cells were sorted for Cre-expression (pTomato fluorescent marker) or expression of an inert control vector. Results: Inactivation of either Dot1l or Mll1 in this model leads to a substantial delay or complete abrogation of leukemia development. Loss of Dot1l or Mll1 are associated with gene expression changes that have substantial overlap. In addition, genes that are downregulated follwing inactivation of Dot1l or Mll1 have substantial overlap with the gene set upregulated in MN1 transduced CMPs. Conclusions: MN1 mediated leukemogenesis is associated with a gene expression program that dependes on Mll1 and Dot1l Examination of mRNA levels between Dot1l f/f and Dot1l ko, and Mll1 f/f and Mll1 ko.

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RNA-seq analysis of murine KMT2A-MLLT3 with DOT1L overexpressed

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RNA sequencing of human CD8+ T cell subsets [TEX]

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