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Acc1 determines memory potential of individual CD4+ T cells by regulating de novo fatty acid biosynthesis

ABSTRACT: Acc1 determines memory potential of individual CD4+ T cells by regulating de novo fatty acid biosynthesis

PROVIDER: PRJNA506713 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7945241.fastq.gz	Fastqsanger.gz
	SRR7945242.fastq.gz	Fastqsanger.gz
	SRR7945243.fastq.gz	Fastqsanger.gz
	SRR7945244.fastq.gz	Fastqsanger.gz

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Similar Datasets

Acc1 determines memory potential of individual CD4+ T cells by regulating de novo fatty acid biosynthesis [microarray]

Project description:Immunological memory is central to adaptive immunity and protection from disease. Changing metabolic demands as antigen-specific T cells transition from effector to memory have been well documented, but the cell-specific pathways and molecules that govern this transition are poorly defined. ACC1 is a rate-limiting enzym in fatty acid biosynthesis. We show that genetic deletion of ACC1 enhanced the formation of CD4+ T cell memory, and that inhibition of ACC1 function enhanced memory T cell formation during parasite infection in mice. ACC1-deficient effector Th cells had similar metabolic signatures to wild-type memory Th cells, and Acaca expression was inversely correlated with a memory gene signature in individual cells. Single cell analysis allowed us to identify a memory precursor-enriched population (CCR7hiCD137lo) present during early differentiation of effector CD4+ T cells. Thus, fatty acid metabolism directs cell fate determination during the generation of memory CD4+ T cells.

2018-11-30 | GSE122861 | GEO

Acc1 determines memory potential of individual CD4+ T cells by regulating de novo fatty acid biosynthesis [RNA-seq]

2018-11-30 | GSE120667 | GEO

Acc1 determines memory potential of individual CD4+ T cells by regulating de novo fatty acid biosynthesis [RT-PCR]

2018-11-30 | GSE122862 | GEO

Acc1 determines memory potential of individual CD4+ T cells by regulating de novo fatty acid biosynthesis [microarray]

Project description:Acc1 determines memory potential of individual CD4+ T cells by regulating de novo fatty acid biosynthesis [microarray]

| PRJNA506715 | ENA

Acc1 determines memory potential of individual CD4+ T cells by regulating de novo fatty acid biosynthesis [RT-PCR]

Project description:Acc1 determines memory potential of individual CD4+ T cells by regulating de novo fatty acid biosynthesis [RT-PCR]

| PRJNA506717 | ENA

Acc1 determines memory potential of individual CD4+ T cells by regulating de novo fatty acid biosynthesis [RNA-seq]

Project description:Acc1 determines memory potential of individual CD4+ T cells by regulating de novo fatty acid biosynthesis [RNA-seq]

| PRJNA494052 | ENA

Acc1 determines memory potential of individual CD4+ T cells by regulating de novo fatty acid biosynthesis

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

2018-11-30 | GSE122863 | GEO

De novo fatty acid synthesis in invariant NKT cells is critical for the development of airway hyperresponsiveness

Project description:Allergic responses in airway against house dust mites (HDMs) depend on lipid metabolism. However, whether the state of lipid metabolism in iNKT cells serves as a critical mechanism to impact development of allergic asthma remains elusive. Here, we showed that acetyl-CoA-Carboxylase 1 (ACC1), a key enzyme for fatty acid synthesis, was highly expressed in iNKT cells from asthmatic lungs. In ovalbumin (OVA)- and HDM-induced allergic asthma models, Cd4-CreAcc1fl/fl mice exhibited impaired homeostasis of iNKT cells and failed to develop AHR. ACC1-deficient iNKT cells reduced intracellular lipid concentration and expression of fatty acid binding proteins (FABPs) and peroxisome proliferator-activated receptor-gamma (PPAR-γ), whereas these cells were increased in glycolytic capacity. Moreover, ACC1-FABP-PPAR-γ axis regulated cell death of ACC1-deficient iNKT cells. Adoptive transfer of wild type (WT) iNKT cells restored AHR in Jɑ18 knockout mice in OVA or HDM-induced asthma models, whereas that of ACC1-deficient iNKT cells did not, indicating that fatty acid synthesis in iNKT cells is one of main contributors to the development of AHR. Our finding demonstrate fatty acid metabolism in iNKT cells is critical contributor for the development of AHR and airway inflammation in asthma.

2022-06-15 | GSE205761 | GEO

ACLY and ACC1 Regulate Hypoxia-Induced Apoptosis by Modulating ETV4 via Î±-ketoglutarate

Project description:In order to propagate a solid tumor, cancer cells must adapt to and survive under various tumor microenvironment (TME) stresses, such as hypoxia or lactic acidosis. To systematically identify genes that modulate cancer cell survival under stresses, we performed genome-wide shRNA screens under hypoxia or lactic acidosis. We discovered that genetic depletion of acetyl-CoA carboxylase (ACACA or ACC1) or ATP citrate lyase (ACLY) protected cancer cells from hypoxia-induced apoptosis. Additionally, loss of ACLY or ACC1 reduced levels and activities of the oncogenic transcription factor ETV4. Silencing ETV4 also protected cells from hypoxia-induced apoptosis and led to remarkably similar transcriptional responses as with silenced ACLY or ACC1, including an anti-apoptotic program. Metabolomic analysis found that while Î±-ketoglutarate levels decrease under hypoxia in control cells, Î±-ketoglutarate is paradoxically increased by hypoxia when ACC1 or ACLY are depleted. Supplementation with Î±-ketoglutarate rescued the hypoxia-induced apoptosis and recapitulated the decreased expression and activity of ETV4 via an epigenetic mechanism. Therefore, ACC1 and ACLY regulate the levels of ETV4 under hypoxia via increased Î±-ketoglutarate. These results reveal that ACC1/ACLY- Î±-ketoglutarate-ETV4 is a novel means by which metabolic states regulate transcriptional output for life vs. death decisions under hypoxia. Since many lipogenic inhibitors are under investigation as cancer therapeutics, our findings suggest that the use of these inhibitors will need to be carefully considered with respect to oncogenic drivers, tumor hypoxia, progression and dormancy. More broadly, our screen provides a framework for studying additional tumor cell stress-adaption mechanisms in the future. DESIGN: H1975 lung cancer cells transduced with a scramble shRNA hairpin or two different shRNAs against ACLY, ACC1, or ETV4 under hypoxia.

2015-12-10 | E-GEOD-61286 | biostudies-arrayexpress

Mitochondrial protein import determines lifespan through metabolic reprogramming and de novo serine biosynthesis.

Project description:Sustained mitochondrial fitness relies on coordinated biogenesis and clearance. Both processes are regulated by constant targeting of proteins into the organelle. Thus, mitochondrial protein import sets the pace for mitochondrial abundance and function. However, our understanding of mitochondrial protein translocation as a regulator of longevity remains enigmatic. Here, we targeted the main protein import translocases and assessed their contribution to mitochondrial abundance and organismal physiology. We find that reduction in cellular mitochondrial load through mitochondrial protein import system suppression, referred to as MitoMISS, elicits a distinct longevity paradigm. We show that MitoMISS triggers the mitochondrial unfolded protein response, orchestrating an adaptive reprogramming of metabolism. Glycolysis and de novo serine biosynthesis are causatively linked to longevity, whilst mitochondrial chaperone induction is dispensable for lifespan extension. Our findings extent the pro-longevity role of UPRmt and provide insight, relevant to the metabolic alterations that promote or undermine survival and longevity.

| S-EPMC8814026 | biostudies-literature

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