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Hippo signaling coordinates cellular quiescence with terminal maturation in iNKT cell development and fate decisions

ABSTRACT: Hippo signaling coordinates cellular quiescence with terminal maturation in iNKT cell development and fate decisions

PROVIDER: PRJNA604829 | ENA |

REPOSITORIES: ENA

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Hippo signaling coordinates cellular quiescence with terminal maturation in iNKT cell development and fate decisions [ClariomS]

Project description:Hippo signaling coordinates cellular quiescence with terminal maturation in iNKT cell development and fate decisions [ClariomS]

| PRJNA604837 | ENA

Hippo signaling coordinates cellular quiescence with terminal maturation in iNKT cell development and fate decisions [MoGene-2_0]

Project description:Hippo signaling coordinates cellular quiescence with terminal maturation in iNKT cell development and fate decisions [MoGene-2_0]

| PRJNA533632 | ENA

Hippo signaling coordinates cellular quiescence with terminal maturation in iNKT cell development and fate decisions [ClariomS]

Project description:Hippo kinases Mst1 and Mst2 act as molecular rheostats for the terminal maturation and effector differentiation programs of iNKT cells. Loss of Mst1 alone or with Mst2 impedes iNKT cell development, associated with defective IL-15-dependent cell survival

2020-04-18 | GSE144776 | GEO

Hippo signaling coordinates cellular quiescence with terminal maturation in iNKT cell development and fate decisions [MoGene-2_0]

Project description:Hippo kinases Mst1 and Mst2 act as molecular rheostats for the terminal maturation and effector differentiation programs of iNKT cells. iNKT developmental stages 1, 2, and 3 (S1, S2, S3) were sorted from the thymus of WT (n = 3) and Cd4CreMst1fl/fl (n = 3) mice

2020-04-07 | GSE130043 | GEO

Hippo/Mst signaling coordinates cellular quiescence with terminal maturation in iNKT cell development and fate decisions.

Project description:Invariant natural killer T (iNKT) cells acquire effector functions during development by mechanisms that remain poorly understood. Here, we show that the Hippo kinases Mst1 and Mst2 act as molecular rheostats for the terminal maturation and effector differentiation programs of iNKT cells. Loss of Mst1 alone or together with Mst2 impedes iNKT cell development, associated with defective IL-15-dependent cell survival. Mechanistically, Mst1 enforces iNKT cellular and transcriptional quiescence associated with maturation and commitment to iNKT1 cells by suppressing proliferation and Opa1-related mitochondrial metabolism that are dynamically regulated during iNKT cell development. Furthermore, Mst1 shapes the reciprocal fate decisions between iNKT1 and iNKT17 effector cells, which respectively depend upon mitochondrial dynamics and ICOS-mTORC2 signaling. Collectively, these findings establish Mst1 as a crucial regulator of mitochondrial homeostasis and quiescence in iNKT cell development and effector lineage differentiation and highlight that establishment of quiescence programs underlies iNKT cell development and effector maturation.

| S-EPMC7971129 | biostudies-literature

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

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

2014-01-27 | GSE51668 | GEO

Hippo signaling coordinates cellular quiescence with terminal maturation in iNKT cell development and fate decisions

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

2020-04-07 | GSE144778 | GEO

Hippo pathway and Bonus control developmental cell fate decisions in the Drosophila eye

Project description:The canonical function of the Hippo signaling pathway is the regulation of organ growth. How this pathway controls cell fate determination is less well understood. Here, we identify a function of the Hippo pathway in cell fate decisions in the developing Drosophila eye, exerted through the interaction of Yorkie (Yki) with the transcriptional regulator Bonus (Bon), an ortholog of mammalian Transcriptional Intermediary Factor 1/tripartite motif (TIF1/TRIM) family proteins. Instead of controlling tissue growth, Yki and Bon promote epidermal and antennal fates at the expense of the eye fate. Proteomic, transcriptomic, and genetic analyses reveal that Yki and Bon control these cell fate decisions by recruiting transcriptional and post-transcriptional co-regulators, and by repressing Notch target genes and activating epidermal differentiation genes. Our work expands the range of functions and regulatory mechanisms under Hippo pathway control.

2023-01-17 | GSE181299 | GEO

iNKT gene profiling_Map3k1

Project description:Transcriptional profiling of iNKT gene expression in Map3k1 control and mutant mice

2016-06-01 | E-MTAB-1561 | biostudies-arrayexpress