Interplay between mitochondria and diet mediates pathogen and stress resistance in Caenorhabditis elegans

dc.citation.articleNumbere1008011en_US
dc.citation.issueNumber3en_US
dc.citation.journalTitlePLoS Geneticsen_US
dc.citation.volumeNumber15en_US
dc.contributor.authorRevtovich, Alexey V.en_US
dc.contributor.authorLee, Ryanen_US
dc.contributor.authorKirienko, Natalia V.en_US
dc.date.accessioned2019-12-11T15:44:19Zen_US
dc.date.available2019-12-11T15:44:19Zen_US
dc.date.issued2019en_US
dc.description.abstractDiet 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.en_US
dc.identifier.citationRevtovich, Alexey V., Lee, Ryan and Kirienko, Natalia V.. "Interplay between mitochondria and diet mediates pathogen and stress resistance in Caenorhabditis elegans." <i>PLoS Genetics,</i> 15, no. 3 (2019) Public Library of Science: https://doi.org/10.1371/journal.pgen.1008011.en_US
dc.identifier.digitaljournal.pgen.1008011en_US
dc.identifier.doihttps://doi.org/10.1371/journal.pgen.1008011en_US
dc.identifier.urihttps://hdl.handle.net/1911/107847en_US
dc.language.isoengen_US
dc.publisherPublic Library of Scienceen_US
dc.rightsThis is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.en_US
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/en_US
dc.titleInterplay between mitochondria and diet mediates pathogen and stress resistance in Caenorhabditis elegansen_US
dc.typeJournal articleen_US
dc.type.dcmiTexten_US
dc.type.publicationpublisher versionen_US
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