- ABC transporter MRP-5 transports vitamin B12 from mother to offspring in C. elegans
- mrp-5 mutant embryonic lethality is rescued by vitamin B12 injection into gonad
- RNAi of mrp-5 reduces S-adenosylmethionine and methionine content in F1 embryos
Vitamin B12 functions as a cofactor for methionine synthase to produce the anabolic methyl donor S-adenosylmethionine (SAM) and for methylmalonyl-CoA mutase to catabolize the short-chain fatty acid propionate. In the nematode Caenorhabditis elegans, maternally supplied vitamin B12 is required for the development of offspring. However, the mechanism for exporting vitamin B12 from the mother to the offspring is not yet known. Here, we use RNAi of more than 200 transporters with a vitamin B12-sensor transgene to identify the ABC transporter MRP-5 as a candidate vitamin B12 exporter. We show that the injection of vitamin B12 into the gonad of mrp-5 deficient mothers rescues embryonic lethality in the offspring. Altogether, our findings identify a maternal mechanism for the transit of an essential vitamin to support the development of the next generation.
Huimin N, Ponomarova O, Giese GE, Walhout AJM. (2018). C. elegans MRP-5 Exports Vitamin B12 from Mother to Offspring to Support Embryonic Development. Cell Reports 22, 3126-3133.