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Updated: Apr 4, 2026
Lipid Supplementation for Longevity and Gene Transcriptional Analysis in Caenorhabditis elegans
Published on: December 9, 2022
Lipid signalling couples translational surveillance to systemic detoxification in Caenorhabditis elegans
J Amaranath Govindan1,2, Elamparithi Jayamani1,3, Xinrui Zhang1
1Department of Molecular Biology, Massachusetts General Hospital, Boston, Massachusetts 02114, USA.
Abstract:
Translation in eukaryotes is followed to detect toxins and virulence factors and coupled to the induction of defence pathways. Caenorhabditis elegans germline-specific mutations in translation components are detected by this system to induce detoxification and immune responses in distinct somatic cells. An RNA interference screen revealed gene inactivations that act at multiple steps in lipid biosynthetic and kinase pathways upstream of MAP kinase to mediate the systemic communication of translation defects to induce detoxification genes. Mammalian bile acids can rescue the defect in detoxification gene induction caused by C. elegans lipid biosynthetic gene inactivations. Extracts prepared from C. elegans with translation deficits but not from the wild type can also rescue detoxification gene induction in lipid-biosynthesis-defective strains. These eukaryotic antibacterial countermeasures are not ignored by bacteria: particular bacterial species suppress normal C. elegans detoxification responses to mutations in translation factors.
Insights
C. elegans detects translation defects to trigger immune responses. Lipid biosynthesis pathways and bile acids are key to this communication, which bacteria can suppress.
Area of Science:
- Molecular Biology
- Cellular Biology
- Immunology
Background:
- Eukaryotic translation is linked to detecting toxins and activating defense pathways.
- C. elegans uses germline translation defects to induce somatic detoxification and immune responses.
Purpose of the Study:
- To investigate the systemic communication of translation defects in C. elegans.
- To identify molecular pathways involved in sensing and responding to translation errors.
Main Methods:
- RNA interference (RNAi) screen to identify genes involved in translation defect signaling.
- Analysis of lipid biosynthetic and kinase pathways upstream of MAP kinase.
- Testing the rescue effects of mammalian bile acids and C. elegans extracts.
Main Results:
- Gene inactivations in lipid biosynthesis and kinase pathways mediate systemic communication of translation defects.
- Mammalian bile acids and C. elegans extracts with translation deficits can rescue detoxification gene induction.
- Specific bacterial species can evade C. elegans detoxification responses to translation factor mutations.
Conclusions:
- A conserved system links translation fidelity to innate immunity in eukaryotes.
- Lipid metabolism and signaling pathways play a crucial role in inter-cellular communication of cellular stress.
- Bacteria have evolved mechanisms to suppress host defense responses targeting translation.
