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ATAC-seq analysis of early T cell progenitors from various gene deficient mice

ABSTRACT: ATAC-seq analysis of early T cell progenitors from various gene deficient mice

PROVIDER: PRJNA1028279 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26387831_1.fastq.gz	Fastqsanger.gz
	SRR26387831_2.fastq.gz	Fastqsanger.gz
	SRR26387832_1.fastq.gz	Fastqsanger.gz
	SRR26387832_2.fastq.gz	Fastqsanger.gz
	SRR26387833_1.fastq.gz	Fastqsanger.gz

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Early T cell progenitors from various gene deficient mice

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Project description:Foxo1 and Ebf1 deficiency leads to a similar disruption of normal B-cell development at the level of the common lymphoid progenitor (CLP). Both mouse strains display the existance of LY6D+ CLPs but a marked/complete lack of proB cells. To investigate similarities of the developmental defects observed we generated gene expression profiles from both genotypes (with corresponding WT controls). This illustrated a shared gene expression signature in Ebf1/Foxo1 deficient CLPs. Gene expression profiling was done using highly purified (FACS sorted) progenitor cells. Cells were purified from bone marrow of wild-type, Foxo1 deficient and Ebf1 deficient mice. Ebf1 deficient bone marrow was aquired by transplantation of Ebf1 deficient progenitors into irradiated hosts. Populations analysed were CLP LY6D-, CLP LY6D+ and proB cells.

2012-11-01 | E-GEOD-41931 | biostudies-arrayexpress

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ATAC-seq of mouse luminal progenitors isolated from wild-type or Blg-Cre;Brca1f/f;p53+/- mouse models

Project description:One of the major hurdles for the early detection of cancer is our poor understanding of tumour initiating events. Historically, cancer research has focused on histological and molecular characterisation of established tumours which has led to the identification of hundreds of putative driver mutations. It is currently unclear how these genetic aberrations impact the cell state of nascent tumour cells and their microenvironment. BRCA1 driven triple negative breast cancer (TNBC) for example has been shown to arise from luminal progenitor cells yet little is known about how BRCA1 loss-of-function (LOF) and concomitant mutations affect the luminal progenitor cell state. This repository contains ATAC-sequencing dataset of luminal progenitors isolated from 6-months old Brca1/p53 and wild-type mice. This data was used to show that the perturbation of Brca1/p53in luminal progenitors induces an aberrant alveolar differentiation pre-malignancy. Unlike alveolar differentiation occurring during gestation, this process is cell autonomous and characterised by the dysregulation of transcription factors driving alveologenesis. The ATAC-sequencing data supports a model where transcriptional and epigenetic changes driven by Brca1/p53 inadvertently promote a differentiation program hardwired in luminal progenitors, highlighting the deterministic role of the cell of origin and offering a potential explanation for the tissue specificity of BRCA1 tumours.

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