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

Abstract

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.

In vitro and in vivo defensive effect of probiotic LAB against Pseudomonas aeruginosa using Caenorhabditis elegans model

“…The influence of selected Lactobacillus strains on colonization in C. elegans was determined using the bacterial colonization assay described by Antunes et al [35], with some modifications. On the first day, lactic acid bacteria were seeded on NGM plates containing worms.…”

“…LAB colonies were quantified and used to calculate the number of bacteria per nematode. The procedure was repeated using P. aeruginosa PA14 as a comparison with lactic acid bacteria [35]. …”

Biochemistry, function, and deficiency of vitamin B12 in Caenorhabditis elegans

“…The B 12 level of the fifth generation worms is only 4% of that in the B 12 -sufficient worms (138 AE 51 ng of B 12 per gram of wet weight). 16 The methylmalonic acid (MMA) and homocysteine (Hcy), which are usually used as the indices of B 12 deficiency, are significantly increased because holo-MCM and -MTR activities are significantly decreased in the worms of the fifth generation grown under B 12 deficiency conditions. 16 These results demonstrate that C. elegans absolutely requires B 12 for growth and develops severe B 12 deficiency when it is grown under B 12 deficiency conditions for five generations.…”

“…16 The methylmalonic acid (MMA) and homocysteine (Hcy), which are usually used as the indices of B 12 deficiency, are significantly increased because holo-MCM and -MTR activities are significantly decreased in the worms of the fifth generation grown under B 12 deficiency conditions. 16 These results demonstrate that C. elegans absolutely requires B 12 for growth and develops severe B 12 deficiency when it is grown under B 12 deficiency conditions for five generations. Such changes in B 12 -dependent enzyme activities are reported to occur in mammals 17,18 ; a B 12 -deficient animal can be produced in only 15 days (five generations) using the nematode model.…”

“…The result suggests that MTR is more susceptible to cellular B 12 levels than MCM. 16 Hepatic MTR activity is mostly derived from the holo-enzyme in B 12 -sufficient or -deficient rats. 17 Although MTR protein levels in liver homogenates of B 12 -deficient rats are significantly reduced compared with those of B 12 -sufficient rats, the hepatic B 12 level does not affect the level of MTR-encoding mRNA.…”