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C. elegans MRP-5 Exports Vitamin B12 from Mother to Offspring to Support Embryonic Development

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 th...

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Detalles Bibliográficos
Autores principales: Na, Huimin, Ponomarova, Olga, Giese, Gabrielle E., Walhout, Albertha J.M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5896776/
https://www.ncbi.nlm.nih.gov/pubmed/29562169
http://dx.doi.org/10.1016/j.celrep.2018.02.100
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author Na, Huimin
Ponomarova, Olga
Giese, Gabrielle E.
Walhout, Albertha J.M.
author_facet Na, Huimin
Ponomarova, Olga
Giese, Gabrielle E.
Walhout, Albertha J.M.
author_sort Na, Huimin
collection PubMed
description 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.
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spelling pubmed-58967762018-04-12 C. elegans MRP-5 Exports Vitamin B12 from Mother to Offspring to Support Embryonic Development Na, Huimin Ponomarova, Olga Giese, Gabrielle E. Walhout, Albertha J.M. Cell Rep Article 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. 2018-03-20 /pmc/articles/PMC5896776/ /pubmed/29562169 http://dx.doi.org/10.1016/j.celrep.2018.02.100 Text en http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Article
Na, Huimin
Ponomarova, Olga
Giese, Gabrielle E.
Walhout, Albertha J.M.
C. elegans MRP-5 Exports Vitamin B12 from Mother to Offspring to Support Embryonic Development
title C. elegans MRP-5 Exports Vitamin B12 from Mother to Offspring to Support Embryonic Development
title_full C. elegans MRP-5 Exports Vitamin B12 from Mother to Offspring to Support Embryonic Development
title_fullStr C. elegans MRP-5 Exports Vitamin B12 from Mother to Offspring to Support Embryonic Development
title_full_unstemmed C. elegans MRP-5 Exports Vitamin B12 from Mother to Offspring to Support Embryonic Development
title_short C. elegans MRP-5 Exports Vitamin B12 from Mother to Offspring to Support Embryonic Development
title_sort c. elegans mrp-5 exports vitamin b12 from mother to offspring to support embryonic development
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5896776/
https://www.ncbi.nlm.nih.gov/pubmed/29562169
http://dx.doi.org/10.1016/j.celrep.2018.02.100
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