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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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p110α of PI3K is Indispensable for Quiescence Exit in Adult Muscle Satellite Cells

Project description:Adult muscle stem cells (MuSC) are quiescent with a localization between myofibers and basal lamina. Upon injury, MuSC exit quiescence, reenter cell cycle, expand and differentiate for muscle regeneration. By using genetic mouse model, we identified p110α/mTORC1 signaling as a indispensable pathway that permits quiescence exit and cell cycle reentry. In order to dig out the downstream effectors, we compared the transcriptome of freshly isolated MuSC from Ctrl (p110α-f/+:R26-YFP/YFP:Pax7-CreER/CreER) to MuSC-specific p110α-null (iKO, p110α-f/f:R26-YFP/YFP:Pax7-CreER/CreER) mice by RNA-sequencing, and AP1 target genes were dramatically down-regulated in iKO MuSC. Restoration of Jun could significantly rescue the cell cycle reentry defect in iKO MuSC. In summary, we provided a p110α/mTORC1/Jun axis required for quiecence exit and cell cycle reentry of MuSC.

2018-02-25 | GSE109472 | GEO

p110α of PI3K is Indispensable for Quiescence Exit in Adult Muscle Satellite Cells

Project description:p110α of PI3K is Indispensable for Quiescence Exit in Adult Muscle Satellite Cells

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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.

2019-03-22 | GSE118619 | GEO

Raptor/mTORC1-dependent metabolic programming of exit from quiescence underlies T cell activation and fate decisions

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.

2014-01-27 | E-GEOD-51668 | biostudies-arrayexpress

Riboproteome remodelling during quiescence exit in Saccharomyces cerevisiae

Project description:Characterization of the riboproteome composition in quiescent cells and post-translational reactivation. To characterize ribosome heterogeneity during the exit from quiescence, the protein composition of ribosomal particles from stationary phase and nutrient-stimulated cells was assessed. A label-free quantitative mass spectrometry strategy was taken to compare quiescent yeast cells with cells that had been nutrient stimulated for 30 and 60 min. To this end, crude extracts from these cells were subjected to sucrose gradient centrifugation and three fractions free (F); monosome (M=80S + 60S + 40S) and polysome (P) were analyzed by nano-HPLC-MS/MS. A total of 528 proteins were identified.

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LRIG1 is a gatekeeper to exit from quiescence in adult neural stem cells

Project description:Adult neural stem cells (NSCs) must tightly regulate quiescence and proliferation. Single cell analysis has suggested a continuum of cell states as NSCs exit quiescence. Here we capture and characterize in vitro primed quiescent NSCs and identify LRIG1 as an important regulator. We show that BMP-4 signaling induces a dormant non-cycling quiescent state (d-qNSCs), whereas combined BMP-4/FGF-2 signalling induces a distinct primed quiescent state poised for cell cycle re-entry. Primed quiescent NSCs (p-qNSCs) are defined by high levels of LRIG1 and CD9, as well as an interferon response signature, and can efficiently engraft into the adult subventricular zone (SVZ) niche. Genetic disruption of Lrig1 in vivo within the SVZ NSCs leads an enhanced proliferation. Mechanistically, LRIG1 primes quiescent NSCs for cell cycle re-entry and EGFR responsiveness by enabling EGFR protein levels to increase but limiting signaling activation. LRIG1 is therefore an important functional regulator of NSC exit from quiescence.

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Raptor/mTORC1-dependent metabolic programming of exit from quiescence underlies T cell activation and fate decisions

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Linking YAP to Müller glia quiescence exit in the degenerative retina

Project description:Linking YAP to Müller glia quiescence exit in the degenerative retina

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MAZ induces MYB expression during the exit from quiescence via the E2F site in the MYB promoter

Project description:Most E2F-binding sites repress transcription through the recruitment of Retinoblasoma (RB) family members until the end of the G1 cell-cycle phase. Although the MYB promoter contains an E2F-binding site, its transcription is activated shortly after the exit from quiescence, before RB family members inactivation, by unknown mechanisms. We had previously uncovered a nuclear factor distinct from E2F, Myb-sp, whose DNA-binding site overlapped the E2F element and had hypothesized that this factor might overcome the transcriptional repression of MYB by E2F-RB family members. We have purified Myb-sp and discovered that Myc-associated zinc finger proteins (MAZ) are major components. We show that various MAZ isoforms are present in Myb-sp and activate transcription via the MYB-E2F element. Moreover, while forced RB or p130 expression repressed the activity of a luciferase reporter driven by the MYB-E2F element, co-expression of MAZ proteins not only reverted repression, but also activated transcription. Finally, we show that MAZ binds the MYB promoter in vivo, that its binding site is critical for MYB transactivation, and that MAZ knockdown inhibits MYB expression during the exit from quiescence. Together, these data indicate that MAZ is essential to bypass MYB promoter repression by RB family members and to induce MYB expression.

2017-10-04 | PXD006857 | Pride

A highly conserved luminal ER exit motif in the pseudoproteases iRhom1 and iRhom2 is indispensable for TNF�� and EGF receptor ligand release

Project description:Membrane-tethered signalling proteins such as TNF�� and many EGF receptor ligands undergo shedding by the metalloproteinase ADAM17 to get released. The pseudoproteases iRhom1 and iRhom2 are important for the ER exit and activity of ADAM17. Yet, their structural requirements to promote ER exit remained unexplored. Utilising in silico and in vitro methods, we here map the conserved iRhom homology domain (IRHD) and provide insights into its structure and function. We identified a highly conserved motif within the IRHD, which is indispensable for the ER exit of iRhoms and termed it CERES (conserved ER exit sequence). Strikingly, single point mutations in CERES abrogate the ER exit without disrupting other iRhom functions. We confirmed the physiological significance of CERES by inactivating it in mice which abrogates ADAM17-mediated shedding ex vivo and in vivo. This demonstrates a crucial role of CERES in the ADAM17-dependent release of various growth factor and cytokine signals.

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