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Microbiota-derived pentanoate promotes differentiation of regulatory T cells via enhancing iron uptake in the intestine [scRNAseq_Treg]

ABSTRACT: Microbiota-derived pentanoate promotes differentiation of regulatory T cells via enhancing iron uptake in the intestine [scRNAseq_Treg]

PROVIDER: PRJNA801476 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17799432_1.fastq.gz	Fastqsanger.gz
	SRR17799432_2.fastq.gz	Fastqsanger.gz
	SRR17799433_1.fastq.gz	Fastqsanger.gz
	SRR17799433_2.fastq.gz	Fastqsanger.gz
	SRR17799434_1.fastq.gz	Fastqsanger.gz

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Microbiota-derived pentanoate promotes differentiation of regulatory T cells via enhancing iron uptake in the intestine.

Project description:Microbiota-derived pentanoate promotes differentiation of regulatory T cells via enhancing iron uptake in the intestine.

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Microbiota-derived pentanoate promotes differentiation of regulatory T cells via enhancing iron uptake in the intestine [Treg_in_vivo]

Project description:Microbiota-derived pentanoate promotes differentiation of regulatory T cells via enhancing iron uptake in the intestine [Treg_in_vivo]

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Microbiota-derived pentanoate promotes differentiation of regulatory T cells via enhancing iron uptake in the intestine [FeSO4_treated_Treg]

Project description:Microbiota-derived pentanoate promotes differentiation of regulatory T cells via enhancing iron uptake in the intestine [FeSO4_treated_Treg]

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Microbiota-derived pentanoate promotes differentiation of regulatory T cells via enhancing iron uptake in the intestine [FeSO4_treated_Treg]

Project description:Iron deficiencies are the most common non-enteric syndromes observed in patients with inflammatory bowel diseases (IBD), yet little is known how iron deficiencies impact immune tolerance in the intestine. The goal of this study is to illuminate role of iron in colonic Treg homeostasis regulation.

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Microbiota-derived pentanoate promotes differentiation of regulatory T cells via enhancing iron uptake in the intestine [scRNAseq_Treg]

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Iron uptake in yeast

Project description:Analysis of iron-regulated gene expression in Saccharomyces cerevisiae using cDNA microarrays has identified three putative cell wall proteins that are directly regulated by Aft1p, the major iron-dependent transcription factor in yeast. FIT1, FIT2, and FIT3 (for facilitator of iron transport) were more highly expressed in strains grown in low concentrations of iron and in strains in which AFT1-1(up), a constitutively active allele of AFT1, was expressed. Northern blot analysis confirmed that FIT1, FIT2, and FIT3 mRNA transcript levels were increased 60-230-fold in response to iron deprivation in an Aft1p-dependent manner. Fit1p was localized exclusively to the cell wall by indirect immunofluorescence. Deletion of the FIT genes, individually or in combination, resulted in diminished uptake of iron bound to the siderophores ferrioxamine B and ferrichrome, without diminishing the uptake of ferric iron salts, or the siderophores triacetylfusarinine C and enterobactin. FIT-deletion strains exhibited increased expression of Aft1p target genes as measured by a FET3-lacZ reporter gene or by Arn1p Western blotting, indicating that cells respond to the absence of FIT genes by up-regulating systems of iron uptake. Aft1p activation in FIT-deleted strains occurred when either ferrichrome or ferric salts were used as sources of iron during growth, suggesting that the FIT genes enhance uptake of iron from both sources. Enzymatic digestion of the cell wall resulted in the release of significant amounts of iron from cells, and the relative quantity of iron released was reduced in FIT-deletion strains. Fit1p, Fit2p, and Fit3p may function by increasing the amount of iron associated with the cell wall and periplasmic space. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set

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Iron uptake experiments in yeast

Project description:The budding yeast S. cerevisiae responds to depletion of iron in the environment by activating Aft1p, the major iron-dependent transcription factor, and by transcribing systems involved in the uptake of iron. Here we have studied the transcriptional response to iron deprivation, and have identified new Aft1p target genes. We find that other metabolic pathways are regulated by iron: biotin uptake and biosynthesis, nitrogen assimilation, and purine biosynthesis. Two enzymes active in these pathways, biotin synthase and glutamate synthase, require an iron-sulfur cluster for activity. Iron deprivation activates transcription of the biotin importer and simultaneously represses transcription of the entire biotin biosynthetic pathway. Multiple genes involved in nitrogen assimilation and amino acid metabolism are induced by iron deprivation, while glutamate synthase, a key enzyme in nitrogen assimilation, is repressed. A CGG palindrome within the promoter of glutamate synthase confers iron-regulated expression, suggesting control by a transcription factor of the binuclear zinc cluster family. We provide evidence that yeast subjected to iron deprivation undergo a transcriptional remodeling, resulting in a shift from iron-dependent to parallel, but iron-independent, metabolic pathways. A dose response design type examines the relationship between the size of the administered dose and the extent of the response of the organism(s). Using regression correlation

2006-02-07 | E-GEOD-4196 | biostudies-arrayexpress

Microbiota-derived pentanoate promotes differentiation of regulatory T cells via enhancing iron uptake in the intestine.

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

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Iron uptake experiments in yeast

2006-02-08 | GSE4196 | GEO