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Transcriptional suppression of sphingolipid catabolism controls pathogen resistance in C. elegans [RNA-Seq]

ABSTRACT: Transcriptional suppression of sphingolipid catabolism controls pathogen resistance in C. elegans [RNA-Seq]

PROVIDER: PRJNA1003630 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25579816_1.fastq.gz	Fastqsanger.gz
	SRR25579816_2.fastq.gz	Fastqsanger.gz
	SRR25579817_1.fastq.gz	Fastqsanger.gz
	SRR25579817_2.fastq.gz	Fastqsanger.gz
	SRR25579818_1.fastq.gz	Fastqsanger.gz

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Transcriptional suppression of sphingolipid catabolism controls pathogen resistance in C. elegans [RNA-Seq]

Project description:Sphingolipids are required for diverse biological functions and are degraded by specific catabolic enzymes. However, the mechanisms that regulate sphingolipid catabolism are not known. Here we characterize a transcriptional axis that regulates sphingolipid breakdown to control resistance against bacterial infection. From an RNAi screen for transcriptional regulators of pathogen resistance in the nematode C. elegans, we identified the nuclear hormone receptor nhr-66, a ligand-gated transcription factor homologous to human hepatocyte nuclear factor 4. Tandem chromatin immunoprecipitation-sequencing (ChIP-seq) and RNA sequencing (RNA-seq) experiments revealed that NHR-66 is a transcriptional repressor, which directly targets sphingolipid catabolism genes. Transcriptional de-repression of two sphingolipid catabolic enzymes in nhr-66 loss-of-function mutants drives the breakdown of sphingolipids, which enhances host susceptibility to infection with the bacterial pathogen Pseudomonas aeruginosa. These data define transcriptional control of sphingolipid catabolism in the regulation of cellular sphingolipids, a process that is necessary for pathogen resistance.

2023-09-08 | GSE240425 | GEO

Transcriptional suppression of sphingolipid catabolism controls pathogen resistance in C. elegans [ChIP-Seq]

2023-09-08 | GSE240426 | GEO

Transcriptional suppression of sphingolipid catabolism controls pathogen resistance in C. elegans

Project description:Transcriptional suppression of sphingolipid catabolism controls pathogen resistance in C. elegans

| PRJNA1003627 | ENA

Transcriptional suppression of sphingolipid catabolism controls pathogen resistance in C. elegans [ChIP-Seq]

Project description:Transcriptional suppression of sphingolipid catabolism controls pathogen resistance in C. elegans [ChIP-Seq]

| PRJNA1003629 | ENA

Transcriptional suppression of sphingolipid catabolism controls pathogen resistance in C. elegans

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

2023-09-08 | GSE240427 | GEO

Intergenerational Neuroprotection by an Intestinal Sphingolipid in Caenorhabditis elegans

Project description:In animals, maternal diet and environment can influence the health of offspring. Whether and how maternal dietary choice impacts the nervous system across multiple generations is not well understood. Here, we show that feeding Caenorhabditis elegans with ursolic acid (UA), a natural plant product, reduces adult-onset neurodegeneration intergenerationally. UA provides neuroprotection by enhancing maternal provisioning of sphingosine-1-phosphate (S1P) - a bioactive sphingolipid. Intestine-to-oocyte S1P transfer is required for intergenerational neuroprotection and is dependent on the RME-2 lipoprotein yolk receptor. S1P acts intergenerationally by upregulating transcription of the acid ceramidase-1 (asah-1) gene in the intestine. Spatially regulating sphingolipid metabolism is critical as inappropriate asah-1 expression in neurons causes developmental axon outgrowth defects. Our results show that sphingolipid homeostasis impacts the development and intergenerational health of the nervous system. The ability of specific lipid metabolites to act as messengers between generations may have broad implications for dietary choice during reproduction.

2023-06-26 | GSE214425 | GEO

Intergenerational Neuroprotection by an Intestinal Sphingolipid in Caenorhabditis elegans

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Oligonucleotide catabolism-derived gluconucleosides in C. elegans

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2023-04-26 | MSV000091804 | MassIVE

Bacterial nucleoside catabolism controls quorum sensing and commensal-to-pathogen transition in the Drosophila gut

Project description:Although gut microbiomes are generally symbiotic or commensal, some of microbiomes become pathogenic under certain circumstances, which is one of key processes of pathogenesis. However, the factors involved in these complex gut-microbe interactions are largely unknown. Here we show that bacterial nucleoside catabolism using gut luminal uridine is required to boost inter-bacterial communications and gut pathogenesis in Drosophila. We found that uridine-derived uracil is required for DUOX-dependent ROS generation on the host side, whereas uridine-derived ribose induces quorum sensing and virulence gene expression on the bacterial side. Importantly, genetic ablation of bacterial nucleoside catabolism is sufficient to block the commensal-to-pathogen transition in vivo. Furthermore, we found that major commensal bacteria lack functional nucleoside catabolism, which is required to achieve gut-microbe symbiosis. The discovery of a novel role of bacterial nucleoside catabolism will greatly help to better understand the molecular mechanism of the commensal-to-pathogen transition in different contexts of host-microbe interactions.

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