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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE240427 | GEO | 2023/09/08

REPOSITORIES: GEO

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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.

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

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

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

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

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

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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]

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

Project description:This SuperSeries is composed of the SubSeries listed below. Keywords: Expression profiling by high throughput sequencing

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Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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Engineering crop Phytophthora resistance by targeting pathogen-derived PI3P for enhanced catabolism.

Project description:Phytophthora pathogens lead to numerous economically damaging plant diseases worldwide, including potato late blight caused by P. infestans and soybean root rot caused by P. sojae. Our previous work showed that Phytophthora pathogens may generate abundant phosphatidylinositol 3-phosphate (PI3P) to promote infection via direct association with RxLR effectors. Here, we designed a disease control strategy for metabolizing pathogen-derived PI3P by expressing secreted Arabidopsis thaliana phosphatidylinositol-4-phosphate 5-kinase 1 (AtPIP5K1), which can phosphorylate PI3P to PI(3,4)P2. We fused AtPIP5K1 with the soybean PR1a signal peptide (SP-PIP5K1) to enable its secretion into the plant apoplast. Transgenic soybean and potato plants expressing SP-PIP5K1 showed substantially enhanced resistance to various P. sojae and P. infestans isolates, respectively. SP-PIP5K1 significantly reduced PI3P accumulation during P. sojae and soybean interaction. Knockout or inhibition of PI3 kinases (PI3Ks) in P. sojae compromised the resistance mediated by SP-PIP5K1, indicating that SP-PIP5K1 action requires a supply of pathogen-derived PI3P. Furthermore, we revealed that SP-PIP5K1 can interfere with the action of P. sojae mediated by the RxLR effector Avr1k. This novel disease control strategy has the potential to confer durable broad-spectrum Phytophthora resistance in plants through a clear mechanism in which catabolism of PI3P interferes with RxLR effector actions.

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Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-07-01 | E-GEOD-71383 | biostudies-arrayexpress

Host pathogen interaction at a transcriptional level

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

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