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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.<\/jats:p>","DOI":"10.7554\/elife.17670","type":"journal-article","created":{"date-parts":[[2016,7,6]],"date-time":"2016-07-06T07:59:50Z","timestamp":1467791990000},"source":"Crossref","is-referenced-by-count":133,"title":["Metabolic network rewiring of propionate flux compensates vitamin B12 deficiency in C. elegans"],"prefix":"10.7554","volume":"5","author":[{"given":"Emma","family":"Watson","sequence":"first","affiliation":[{"name":"Program in Systems Biology, University of Massachusetts Medical School, Worcester, United States"},{"name":"Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Viridiana","family":"Olin-Sandoval","sequence":"additional","affiliation":[{"name":"Department of 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