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

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

PROVIDER: PRJNA577713 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10285408.fastq.gz	Fastqsanger.gz
	SRR10285409.fastq.gz	Fastqsanger.gz
	SRR10285410.fastq.gz	Fastqsanger.gz
	SRR10285411.fastq.gz	Fastqsanger.gz
	SRR10285412.fastq.gz	Fastqsanger.gz

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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.

2020-11-19 | GSE138909 | GEO

H3K79me2 naïve and in vitro activated B cells

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.

2020-11-19 | GSE138906 | GEO

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

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.

2016-01-12 | E-GEOD-76748 | biostudies-arrayexpress

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.

2021-08-01 | GSE155406 | GEO

The Histone Methyltransferases MLL1 and DOT1L Cooperate with Meningioma-1 to Induce AML [Mouse Mll1 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.

2016-01-12 | E-GEOD-76749 | biostudies-arrayexpress

H3K79me2 naïve and in vitro activated B cells

Project description:H3K79me2 naïve and in vitro activated B cells

| PRJNA577712 | ENA

Whole lung gene expression from naïve Bpifb1 WT and KO mice

Project description:We performed RNAsequencing on whole lung tissue from naïve Bpifb1 WT and KO mice.

2020-09-01 | GSE150452 | GEO

RNA expression in WT and Dot1L KO CD8 T cell subsets

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

| PRJNA577714 | ENA

DOT1L regulates chromatin reorganization and gene expression during sperm differentiation

Project description:Spermatozoa have a unique genome organization: their chromatin is almost completely devoid of histones and is formed instead of protamines which confer a high level of compaction and preserve paternal genome integrity until fertilization. Histone-to-protamine transition takes place in spermatids and is indispensable for the production of functional sperm. Here we show that the H3K79-methyltransferase DOT1L controls spermatid chromatin remodelling and subsequent reorganization and compaction of spermatozoon genome. Using a mouse model in which Dot1l is knocked-out (KO) in postnatal male germ cells, we found that Dot1l-KO sperm chromatin is less compact and has an abnormal content, characterized by the presence of transition proteins, immature protamine 2 forms and a higher level of histones. Proteomics and transcriptomics analyses performed on spermatids reveal that Dot1l-KO modifies the chromatin prior to histone removal, and leads to the deregulation of genes involved in flagellum formation and apoptosis during spermatid differentiation. As a consequence of these chromatin and gene expression defects, Dot1l-KO spermatozoa have less compact heads and are less motile, which results in impaired fertility.

2023-03-30 | PXD030734 | Pride

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