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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE140224 | GEO | 2020/03/05

REPOSITORIES: GEO

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

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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.

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

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.

2012-09-19 | E-GEOD-32265 | biostudies-arrayexpress

Response to salt stress of Raptor mutants

Project description:ra12-03_raptor-nacl - Characterization to raptor mutants (partner of the kinase TOR) and of their answer to the salt stress. - Sowing on metal grids on MS/2 medium with continuous light. Transfer after 12 days of culture for 3h to liquid MS/2 medium containing or not 200 mM NaCl. 7 dye-swap - gene knock out, treated vs untreated comparison

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Ribosome profiling of metformin treatment in primary murine hepatocytes in WT, Raptor Ser-Ala mutant, Tsc2-null, Raptor mutant;Tsc2-null, and Ampk-null cells

Project description:Despite being the frontline therapy for Type 2 diabetes, the mechanisms of action of the biguanide drug metformin are still being discovered. In particular, the detailed molecular interplays between the AMPK and the mTORC1 pathway in the hepatic benefits of metformin are still ill-defined. Metformin-dependent activation of AMPK classically inhibits mTORC1 via TSC/RHEB. But several lines of evidence suggest additional mechanisms at play in metformin inhibition of mTORC1. Here we investigated the role of direct AMPK-mediated serine phosphorylation of RAPTOR in a new RaptorAA mouse model, in which AMPK phospho-serine sites Ser722 and Ser792 of RAPTOR were mutated to alanine. Metformin treatment of primary hepatocytes and intact murine liver requires AMPK regulation of both RAPTOR and TSC2 to fully inhibit mTORC1, and this regulation is critical for the translational response to metformin.

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

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

| PRJNA541439 | ENA

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

2014-01-27 | GSE51668 | GEO

RNA-seq of metformin treatment in primary murine hepatocytes in WT, Raptor Ser-Ala mutant, Tsc2-null, Raptor mutant;Tsc2-null, and Ampk-null cells

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Response to salt stress of Raptor mutants

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