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Bacterial pattern recognition in C. elegans by the nuclear hormone receptor NHR-86/HNF4

ABSTRACT: Bacterial pattern recognition in C. elegans by the nuclear hormone receptor NHR-86/HNF4

PROVIDER: PRJNA835140 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19088018.fastq.gz	Fastqsanger.gz
	SRR19088019.fastq.gz	Fastqsanger.gz
	SRR19088020.fastq.gz	Fastqsanger.gz
	SRR19088021.fastq.gz	Fastqsanger.gz
	SRR19088022.fastq.gz	Fastqsanger.gz

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Bacterial pattern recognition in C. elegans by the nuclear hormone receptor NHR-86/HNF4

Project description:Pattern recognition of bacterial products by host receptors is essential for pathogen sensing in many metazoans. Caenorhabditis elegans, however, do not utilize canonical pattern recognition receptors to activate innate immunity toward bacterial pathogens. Whether other mechanisms evolved in nematodes to directly sense pathogens is not known. Here, we characterize the first bacterial pattern recognition receptor and its natural ligand in C. elegans. We show that the C. elegans nuclear hormone receptor NHR-86/HNF4 senses phenazine-1-carboxamide (PCN), a metabolite produced by pathogenic strains of Pseudomonas aeruginosa, to activate protective anti-pathogen defenses in the intestine. PCN binds to the ligand binding domain of NHR-86/HNF4, a ligand-gated transcription factor, which engages a transcriptional program in intestinal epithelial cells that promotes metabolism of toxic phenazines to provide protection against P. aeruginosa. These data de-orphan a nuclear hormone receptor and demonstrate that sensing a metabolite signal of bacterial virulence allows nematodes to detect pathogens in its environment that are poised to cause disease.

2023-02-07 | GSE202258 | GEO

The nuclear hormone receptor NHR-86 controls anti-pathogen responses in C. elegans [ChIP-seq]

Project description:Germline-encoded pattern recognition receptors (e.g. Toll-like receptors) play key roles in innate immune activation. However, some metazoans, such as C. elegans, do not have canonical mechanisms of pattern recognition, yet they are able to mount anti-pathogen immune defenses. Here, we demonstrate that a nuclear hormone receptor (NHR), a ligand-gated transcription factor, functions in immune activation and pathogen defense. NHRs have expanded dramatically in C. elegans compared to other metazoans. Because NHRs often function redundantly, it has been challenging experimentally to characterize the biology of individual NHRs. Here, we use genetic epistasis experiments, transcriptome profiling analyses and chromatin immunoprecipitation to show NHR-86 is sufficient to activate protective immune defenses against the bacterial pathogen Pseudomonas aeruginosa. Interestingly, NHR-86 drives the transcription of immune effectors whose basal regulation requires the canonical p38 MAPK PMK-1 immune pathway. However, NHR-86 functions independently of PMK-1 and directly induces the transcription of infection response genes in a manner that confers protection from bacterial infection. Importantly, we found that nhr-86 does control immune gene expression and is necessary for host defense against a different pathogen, Enterococcus faecalis. Our findings characterize an ancient role of an NHR in innate immunity, and suggest that the expansion of the NHR protein family in C. elegans has been fueled in part by the need to activate immune defenses in response to pathogen attack.

2019-01-09 | GSE117719 | GEO

The nuclear hormone receptor NHR-86 controls anti-pathogen responses in C. elegans [RNA-seq]

2019-01-09 | GSE117700 | GEO

NHR-49/HNF4 integrates regulation of fatty acid metabolism with a protective transcriptional response to oxidative stress and fasting

Project description:Endogenous and exogenous stresses elicit transcriptional responses that limit damage and promote cell/organismal survival. Like its mammalian counterparts, Hepatocyte Nuclear Factor 4 (HNF4) and peroxisome proliferator-activated receptor a (PPARa), Caenorhabditis elegans NHR-49 is a well-established regulator of lipid metabolism. Here, we reveal that NHR-49 is essential to activate a transcriptional response common to organic peroxide and fasting, which includes the pro-longevity gene fmo-2/flavin-containing monoxygenase. These NHR-49-dependent, stress-responsive genes are also upregulated in long-lived glp-1/notch receptor mutants, and two of them contribute to increased oxidative stress resistance in wild-type worms and long-lived glp-1 mutants. Similar to its role in lipid metabolism, NHR-49 requires the Mediator subunit mdt-15 to promote stress-induced gene expression. However, NHR-49 acts independently from the transcription factor hlh-30/TFEB that also promotes fmo-2 expression. Similarly, activation of the p38 MAPK, PMK-1, which is important for adaptation to a variety of stresses, is only important for peroxide-induced expression of a subset of NHR-49-dependent genes, including fmo-2. Notably, we find that organic peroxide increases NHR-49 protein levels, apparently by a post-transcriptional mechanism that does not require PMK-1 activation. Together these findings establish a new role for the HNF4/PPARa-related NHR-49 as a stress-activated regulator of cytoprotective gene expression.

2018-03-05 | GSE107799 | GEO

The nuclear hormone receptor NHR-86 controls anti-pathogen responses in C. elegans

Project description:The nuclear hormone receptor NHR-86 controls anti-pathogen responses in C. elegans

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The nuclear hormone receptor NHR-86 controls anti-pathogen responses in C. elegans [RNA-seq]

Project description:The nuclear hormone receptor NHR-86 controls anti-pathogen responses in C. elegans [RNA-seq]

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The nuclear hormone receptor NHR-86 controls anti-pathogen responses in C. elegans [ChIP-seq]

Project description:The nuclear hormone receptor NHR-86 controls anti-pathogen responses in C. elegans [ChIP-seq]

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RNA-Sequencing used to identify the targets of NHR-49, a transcription factor that acts in distinct tissues to promote longevity versus immunity

Project description:Previously, we identified NHR-49, functional homolog of the key vertebrate lipid metabolism regulator HNF4/PPARa, as essential for the longevity of Germiline Strem Cell (GSC)-less animals. Since longevity and stress resistance have been reported to be strongly linked, we examined the role of NHR-49 in resistance against the human opportunistic pathogen Pseudomonas aeruginosa, strain PA14. As a part of this effort we employed RNA-Sequencing to determine the downstream targets of NHR-49 in GSC-less animals.

2020-09-30 | GSE158729 | GEO

The nuclear hormone receptor NHR-86 controls anti-pathogen responses in C. elegans.

Project description:Nuclear hormone receptors (NHRs) are ligand-gated transcription factors that control adaptive host responses following recognition of specific endogenous or exogenous ligands. Although NHRs have expanded dramatically in C. elegans compared to other metazoans, the biological function of only a few of these genes has been characterized in detail. Here, we demonstrate that an NHR can activate an anti-pathogen transcriptional program. Using genetic epistasis experiments, transcriptome profiling analyses and chromatin immunoprecipitation-sequencing, we show that, in the presence of an immunostimulatory small molecule, NHR-86 binds to the promoters of immune effectors to activate their transcription. NHR-86 is not required for resistance to the bacterial pathogen Pseudomonas aeruginosa at baseline, but activation of NHR-86 by this compound drives a transcriptional program that provides protection against this pathogen. Interestingly, NHR-86 targets immune effectors whose basal regulation requires the canonical p38 MAPK PMK-1 immune pathway. However, NHR-86 functions independently of PMK-1 and modulates the transcription of these infection response genes directly. These findings characterize a new transcriptional regulator in C. elegans that can induce a protective host response towards a bacterial pathogen.

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C. elegans: wildtype vs nhr-49-/-; wildtype vs nhr-66-/-; wildtype vs nhr-80-/-

Project description:Transcriptional profiling of C. elegans NHR-49, NHR-66 and NHR-80

2012-03-15 | GSE34856 | GEO