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Impact of Tle1, Tle3, and Tle4 deficiency on hematopoietic stem cells (HSCs) [RNA-seq]

ABSTRACT: Impact of Tle1, Tle3, and Tle4 deficiency on hematopoietic stem cells (HSCs) [RNA-seq]

PROVIDER: PRJNA521469 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8550060.fastq.gz	Fastqsanger.gz
	SRR8550060_1.fastq.gz	Fastqsanger.gz
	SRR8550060_2.fastq.gz	Fastqsanger.gz
	SRR8550061_1.fastq.gz	Fastqsanger.gz
	SRR8550061_2.fastq.gz	Fastqsanger.gz

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Impact of Tle1, Tle3, and Tle4 deficiency on hematopoietic stem cells (HSCs) [RNA-seq]

Project description:To compare the transcriptomes between control and Tle1/3/4-deficient HSCs Tle co-repressors can co-opt a number of transcription factors to repress target gene expression. Due to gene duplication during evolution, there are 4 Tle genes in mammalian genome, and their functional redundancy has a major hurdle to understand their roles in hematopoietic stem cells (HSCs). Here we used Vav-Cre to ablate Tle1, 3, and 4 genes in HSCs, and performed RNA-seq to determine the impact of Tle deficiency on HSCs. To further define the regulatory mechanisms, we performed Tle3 ChIPseq on c-Kit+ hematopoietic progenitor cells. The data obtained collectively indicate a critical, intrinsic requirement for Tle corepressors in HSC self-renewal.

2020-02-01 | GSE126271 | GEO

Genome-wide maps of Tle3 binding in hematopoietic progenitor cells [ChIP-seq]

Project description:To determine Genome-wide Tle3 binding locations in c-Kit+ mouse bone marrow cells Tle co-repressors can co-opt a number of transcription factors to repress target gene expression. Due to gene duplication during evolution, there are 4 Tle genes in mammalian genome, and their functional redundancy has a major hurdle to understand their roles in hematopoietic stem cells (HSCs). Here we used Vav-Cre to ablate Tle1, 3, and 4 genes in HSCs, and performed RNA-seq to determine the impact of Tle deficiency on HSCs. To further define the regulatory mechanisms, we performed Tle3 ChIPseq on c-Kit+ hematopoietic progenitor cells. The data obtained collectively indicate a critical, intrinsic requirement for Tle corepressors in HSC self-renewal.

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Impact of Tle3 deficiency on memory T cell transcriptome

Project description:Impact of Tle3 deficiency on memory T cell transcriptome

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Impact of Tle3 deficiency on memory T cell chromatin accessbility landscape

Project description:Impact of Tle3 deficiency on memory T cell chromatin accessbility landscape

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Impact of Tcf1 and Lef1 deficiency on HSCs

Project description:Comparison of transcriptome between control and Tcf1/Lef1-deficient hematopoietic stem cells (HSCs).

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Impact of Tle3 deficiency on memory T cell transcriptome

Project description:The goal of this study is to determine if central memory (Tcm) and effector memory (Tem) CD8 T cells can be reprogrammed to change their fate. We demonstrate that genetic ablation of Tle3 can promote generation of Tcm cells at the expense of Tem cells, and this can occur during the effector phase of the immune response.

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Genome-wide maps of Tle3 binding and Tle1/3/4 deficiency on hematopoietic stem cells

Project description:Genome-wide maps of Tle3 binding and Tle1/3/4 deficiency on hematopoietic stem cells

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Impact of Tle3 deficiency on memory T cell chromatin accessbility landscape

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RNA-seq to assess the impact of circulation on hematopoietic stem cell differentiation.

Project description:Blood flow promotes hematopoiesis, Definitive hematopoietic stem cells can not be assessed in circulation negative Ncx-/- mice. This study looks at the impact of lack of blood flow on the earliest blood cell precursors, the pro-HSCs. E9.5 was chosen as this is the time point pro-HSCs are normally generated. Cells from the hemogenic endothelium, the endothelium and pro-HSCs were sequenced.

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Adipose subtype-selective recruitment of TLE3 in thermogenic gene programs

Project description:Transcriptional effectors of white adipocyte-selective gene expression have not been described. TLE3 is a white-selective cofactor that acts reciprocally with the brown-selective cofactor Prdm16 to specify lipid storage and thermogenic gene programs. When expressed at elevated levels in brown fat, TLE3 counters Prdm16, suppressing brown-selective genes and inducing white-selective genes, resulting in impaired fatty acid oxidation and thermogenesis. To further test the functional consequences of the changes in BAT phenotype in aP2-TLE3 Tg mice, we challenged them with cold exposure at 4C. aP2-TLE3 Tg mice had an impaired ability to respond to cold exposure compared to littermate control mice, as evidenced by a marked drop in core body temperature. Transgenic mice expressing TLE3 from the aP2 enhancer and wild type mice were housed individually without food and bedding immediately before the start of experiments. Mice were allowed free access to water and placed at 4C for 5 hours while core body temperature was monitored every hour using a rectal probe. For microarray experiments of BAT, RNA was extracted and pooled from 4 mice in each group.

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