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FEBS Open Bio. 2013 Feb 1;3:112-7. doi: 10.1016/j.fob.2013.01.008. Print 2013.

Vitamin B12 deficiency in Caenorhabditis elegans results in loss of fertility, extended life cycle, and reduced lifespan.

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Division of Applied Bioresources Chemistry, The United Graduate School of Agricultural Sciences, Tottori University, Tottori, Japan.


Vitamin B12 (B12) deficiency has been linked to developmental disorders, metabolic abnormalities, and neuropathy; however, the mechanisms involved remain poorly understood. Caenorhabditis elegans grown under B12-deficient conditions for five generations develop severe B12 deficiency associated with various phenotypes that include decreased egg-laying capacity (infertility), prolonged life cycle (growth retardation), and reduced lifespan. These phenotypes resemble the consequences of B12 deficiency in mammals, and can be induced in C. elegans in only 15 days. Thus, C. elegans is a suitable animal model for studying the biological processes induced by vitamin deficiency.


Ado-B12, 5′-deoxyadenosylcobalamin; B12, vitamin B12; C. elegans, Caenorhabditis elegans; CH3-B12, methylcobalamin; Caenorhabditis elegans; Cobalamin; Hcy, homocysteine; MCM, methylmalonyl-CoA mutase; MMA, methylmalonic acid; MS, methionine synthase.; Methionine synthase; Methylmalonic acid; Methylmalonyl-CoA mutase; Vitamin B12

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