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Raptor determines β-cell identity and plasticity independent of metabolic state

ABSTRACT: Raptor determines β-cell identity and plasticity independent of metabolic state

PROVIDER: PRJNA541439 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9021720_1.fastq.gz	Fastqsanger.gz
	SRR9021720_2.fastq.gz	Fastqsanger.gz
	SRR9021721_1.fastq.gz	Fastqsanger.gz
	SRR9021721_2.fastq.gz	Fastqsanger.gz
	SRR9021712_1.fastq.gz	Fastqsanger.gz

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Raptor determines β-cell identity and plasticity independent of metabolic state

Project description:In this study, we employed RNA-seq technology to identify the exact role of mTORC1 on β-cell identity and plasticity.

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Raptor determines ?-cell identity and plasticity independent of hyperglycemia in mice.

Project description:Compromised ?-cell identity is emerging as an important contributor to ?-cell failure in diabetes; however, the precise mechanism independent of hyperglycemia is under investigation. We have previously reported that mTORC1/Raptor regulates functional maturation in ?-cells. In the present study, we find that diabetic ?-cell specific Raptor-deficient mice (?RapKOGFP) show reduced ?-cell mass, loss of ?-cell identity and acquisition of ?-cell features; which are not reversible upon glucose normalization. Deletion of Raptor directly impairs ?-cell identity, mitochondrial metabolic coupling and protein synthetic activity, leading to ?-cell failure. Moreover, loss of Raptor activates ?-cell transcription factor MafB (via modulating C/EBP? isoform ratio) and several ?-cell enriched genes i.e. Etv1 and Tspan12, thus initiates ?- to ?-cell reprograming. The present findings highlight mTORC1 as a metabolic rheostat for stabilizing ?-cell identity and repressing ?-cell program at normoglycemic level, which might present therapeutic opportunities for treatment of diabetes.

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Cellular plasticity upon proton irradiation determines tumor cell radiosensitivity

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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.

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Gene-expression changes resulting from loss of the mTORC1 component Raptor in murine hematopoietic stem and progenitor cell-enriched populations (HSPC)

Project description:We investigated the role of mTORC1 in murine hematopoiesis by conditionally deleting the Raptor gene in murine hematopoietic stem cells. We observed mutliple alterations evoked by Raptor loss in hematopoiesis and profiled gene-expression alterations induced by raptor loss in Flt3-Lin-Sca1+cKit+ hematopoietic stem and progenitor enriched cell populations, 5 weeks post Raptor deletion. Flt3-Lin-Sca1+cKit+ cells were flow sorted from mice containing homozygous floxed alleles for exon 6 of the Raptor gene in the presence (MT group) or absence (WT group) of the MxCre transgene, which was induced with injections of mice with pIpC 5 weeks before cell isolation.

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Raptor is required for β-cell metabolic coupling and repressing an α cell program before onset of hyperglycemia

Project description:Raptor deficient mice showed diabetic phenotype, to dissect the effect of hyperglycemia, we isolated euglycemic 2-week-old β cells to perform microarray. To determine the influence of Raptor deficiency on β cells independent of hyperglycemia, we hace employed whole transcriptome expression profiling as a discovery platform to identify differentially expressed genes compared with wild type controls. We isolated mice islets, then disgested them into single cells by 0.25% EDTA, and sorted for GFP by FACS.

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