ArticlePLoS pathogens2023
Transcriptional suppression of sphingolipid catabolism controls pathogen resistance in C. elegans.
Article in PLoS pathogens, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
12 citing papers in PubMed, 10 citations in OpenAlex.
- Life-History, Stress-Resistance, and Transcriptomic Variation Among a MexicanEcology and evolution · 2026Article
- Intestinal lipid metabolism controls molecular and behavioral immunity through NHR-68 and gut-brain signaling in Caenorhabditis elegans.PLoS biology · 2026Article
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- Worming out defence strategies: mechanisms of immunity through the lens of genetic screens in C. elegans.Heredity · 2026Review
- Fungal Sphingolipids: Biosynthesis Pathways, Structural Features and Biological Functions.Journal of fungi (Basel, Switzerland) · 2026Review
- Caenorhabditis elegans as an experimental model for resilience-boosting microbiota interventions in nonmodel ectotherms.FEMS microbiology reviews · 2026Review
- Patterns of pathogenesis in innate immunity: insights from C. elegans.Nature reviews. Immunology · 2025Review
- Cuticular collagens mediate cross-kingdom predator-prey interactions between trapping fungi and nematodes.PLoS biology · 2025Article
- Polyketide synthase-derived sphingolipids mediate microbiota protection against a bacterial pathogen in C. elegans.Nature communications · 2025Article
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- The MAB-5/Hox family transcription factor is important for Caenorhabditis elegans innate immune response to Staphylococcus epidermidis infection.G3 (Bethesda, Md.) · 2024Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
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 and RNA sequencing 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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Registered trials
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