ArticleeLife2016
Metabolic network rewiring of propionate flux compensates vitamin B12 deficiency in C. elegans.
Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
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Who cites it
76 citing papers in PubMed, 134 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
- Bacteria producing the bioplastic polyhydroxybutyrate kill the nematode Caenorhabditis elegans.PLoS biology · 2026Article
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- Animal models of methylmalonic acidemia: insights and challenges.Orphanet journal of rare diseases · 2025Review
- A simple, fast and inexpensive approach using E. coli to detect and estimate vitamin B12 content in microbial extracts.Biology open · 2025Article
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- Germline status and micronutrient availability regulate a somatic mitochondrial quality control pathway via short-chain fatty acid metabolism.bioRxiv : the preprint server for biology · 2024Article
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16 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Metabolic network rewiring is the rerouting of metabolism through the use of alternate enzymes to adjust pathway flux and accomplish specific anabolic or catabolic objectives. Here, we report the first characterization of two parallel pathways for the breakdown of the short chain fatty acid propionate in Caenorhabditis elegans. Using genetic interaction mapping, gene co-expression analysis, pathway intermediate quantification and carbon tracing, we uncover a vitamin B12-independent propionate breakdown shunt that is transcriptionally activated on vitamin B12 deficient diets, or under genetic conditions mimicking the human diseases propionic- and methylmalonic acidemia, in which the canonical B12-dependent propionate breakdown pathway is blocked. Our study presents the first example of transcriptional vitamin-directed metabolic network rewiring to promote survival under vitamin deficiency. The ability to reroute propionate breakdown according to B12 availability may provide C. elegans with metabolic plasticity and thus a selective advantage on different diets in the wild.
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Registered trials
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