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Foxp1 is indispensable for ductal morphogenesis and controls the exit of mammary stem cells from quiescence [RNA-seq and ChIP-seq]

ABSTRACT: Foxp1 is indispensable for ductal morphogenesis and controls the exit of mammary stem cells from quiescence [RNA-seq and ChIP-seq]

PROVIDER: PRJNA486262 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7701130.fastq.gz	Fastqsanger.gz
	SRR7701140.fastq.gz	Fastqsanger.gz
	SRR7701150.fastq.gz	Fastqsanger.gz
	SRR7701131.fastq.gz	Fastqsanger.gz
	SRR7701141.fastq.gz	Fastqsanger.gz

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Project description:Long-lived quiescent mammary stem cells (MaSCs) are presumed to coordinate the dramatic expansion of ductal epithelium that occurs through the different phases of postnatal development, but little is known about the molecular regulators that underpin the activation of MaSCs. Here we show that ablation of the transcription factor Foxp1 in the mammary gland profoundly impairs ductal morphogenesis, resulting in a rudimentary tree throughout adult life. Foxp1-deficient glands were highly enriched for quiescent Tspan8hi MaSCs, which failed to become activated, even in competitive transplantation assays, and therefore harbor a cell-intrinsic defect. Luminal cells aberrantly expressed basal genes, suggesting that Foxp1 may also contribute to cell-fate decisions. Notably, Foxp1 was uncovered as a direct repressor of the Tspan8 gene in basal cells and deletion of Tspan8 could rescue the profound defects in ductal morphogenesis elicited by Foxp1 loss. Thus, a single transcriptional regulator, Foxp1, can control the exit of MaSCs from dormancy to orchestrate differentiation and development.

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Project description:Naïve T cells respond to antigen stimulation by exiting from quiescence into clonal expansion and functional differentiation, but the control mechanism is elusive. Here we describe that Raptor/mTORC1-dependent metabolic reprogramming is a central determinant of this transitional process. Loss of Raptor abrogates T cell priming and Th2 cell differentiation, although Raptor function is less important for continuous proliferation of actively cycling cells. mTORC1 coordinates multiple metabolic programs in T cells including glycolysis, lipid synthesis and oxidative phosphorylation to mediate antigen-triggered exit from quiescence. mTORC1 further links glucose metabolism to the initiation of Th2 differentiation by orchestrating cytokine receptor expression and cytokine responsiveness. Activation of Raptor/mTORC1 integrates T cell receptor (TCR) and CD28 co-stimulatory signals in antigen-stimulated T cells. Our studies identify a Raptor/mTORC1-dependent pathway linking signal-dependent metabolic reprogramming to quiescence exit, and this in turn coordinates lymphocyte activation and fate decisions in adaptive immunity. We used microarrays to explore the gene expression profiles differentially expressed in CD4+ T-cells from wild-type (WT) and CD4(cre) x Raptor(fl/fl) mice before and after stimulation with anti CD3/CD28 antibodies.

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Foxp1 is indispensable for ductal morphogenesis and controls the exit of mammary stem cells from quiescence [RNA-seq and ChIP-seq]

Project description:This SuperSeries is composed of the SubSeries listed below.

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