ArticlePLoS genetics2019
Interplay between mitochondria and diet mediates pathogen and stress resistance in Caenorhabditis elegans.
Article in PLoS genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed, 100 citations in OpenAlex.
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- SIN-3 coregulator maintains adaptive capacity to different diets in Caenorhabditis elegans through vitamin B12.G3 (Bethesda, Md.) · 2026Article
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- Effects of Methylcobalamin on Mitochondrial Alterations in Schwann Cells Under Oxidative Stress.Biomedicines · 2025Article
- Bacterial RNA promotes proteostasis through inter-tissue communication in C. elegans.Nature communications · 2025Article
- Cross-comparison of strains used for mitochondrial imaging inLife science alliance · 2025Article
- Targeting phospholipase PLAG-15 promotes healthy aging iniScience · 2025Article
- A new class of natural anthelmintics targeting lipid metabolism.Nature communications · 2025Article
- Piwi mutant germ cells transmit a form of heritable stress that promotes longevity.Aging cell · 2025Article
- Regulation of Caenorhabditis elegans HLH-30 subcellular localization dynamics: Evidence for a redox-dependent mechanism.Free radical biology & medicine · 2024Article
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- Bacteria-organelle communication in physiology and disease.The Journal of cell biology · 2024Review
5 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Diet is a crucial determinant of organismal biology; interactions between the host, its diet, and its microbiota are critical to determining the health of an organism. A variety of genetic and biochemical means were used to assay stress sensitivity in C. elegans reared on two standard laboratory diets: E. coli OP50, the most commonly used food for C. elegans, or E. coli HT115, which is typically used for RNAi-mediated gene knockdown. We demonstrated that the relatively subtle shift to a diet of E. coli HT115 had a dramatic impact on C. elegans's survival after exposure to pathogenic or abiotic stresses. Interestingly, this was independent of canonical host defense pathways. Instead the change arises from improvements in mitochondrial health, likely due to alleviation of a vitamin B12 deficiency exhibited by worms reared on an E. coli OP50 diet. Increasing B12 availability, by feeding on E. coli HT115, supplementing E. coli OP50 with exogenous vitamin B12, or overexpression of the B12 transporter, improved mitochondrial homeostasis and increased resistance. Loss of the methylmalonyl-CoA mutase gene mmcm-1/MUT, which requires vitamin B12 as a cofactor, abolished these improvements, establishing a genetic basis for the E. coli OP50-incurred sensitivity. Our study forges a mechanistic link between a dietary deficiency (nutrition/microbiota) and a physiological consequence (host sensitivity), using the host-microbiota-diet framework.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.