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Here we show that the conserved SIN3 transcriptional coregulator is required in Caenorhabditis elegans for animals to adapt to different bacterial diets. Shifting sin-3 mutant animals from the commonly used E. coli \u00a0OP50 strain to the E. coli \u00a0HT115 strain used for RNAi knockdown experiments has a dramatic impact on survival, leading to the lethality of mutant animals at the young adult stage. A major difference between OP50 and HT115 is vitamin B12 content, which is lower in OP50 than HT115. Feeding sin-3 mutant animals on OP50 bacteria supplemented with vitamin B12 reproduced the lethality observed on HT115. Vitamin B12 functions in 2 metabolic pathways: the canonical propionate breakdown pathway and the methionine\/S-adenosylmethionine (met\/SAM) cycle. Loss of metr-1, encoding the methionine synthase enzyme that requires vitamin B12 as a cofactor in the met\/SAM cycle repressed lethality on HT115. Conversely, complementation with metabolites of the met\/SAM cycle enhanced lethality on OP50. These results show that SIN-3 is required for animals to adapt to dietary changes through B12-dependent metabolic pathways.<\/jats:p>","DOI":"10.1093\/g3journal\/jkag087","type":"journal-article","created":{"date-parts":[[2026,4,13]],"date-time":"2026-04-13T02:18:17Z","timestamp":1776046697000},"source":"Crossref","is-referenced-by-count":0,"title":["SIN-3 coregulator maintains adaptive capacity to different diets in\n                    <i>Caenorhabditis elegans<\/i>\n                    through vitamin B12"],"prefix":"10.1093","volume":"16","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3087-449X","authenticated-orcid":false,"given":"Francesca","family":"Palladino","sequence":"first","affiliation":[{"name":"Laboratory of Biology and Modeling of the Cell, UMR5239 CNRS\/Ecole Normale Sup\u00e9rieure de Lyon, INSERM U1210, UMS 3444 Biosciences Lyon Gerland, Universit\u00e9 de Lyon , 46 all\u00e9e d'Italie Lyon 69007 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