Magnesium Excretion in C. elegans Requires the Activity of the GTL-2 TRPM Channel

Systemic magnesium homeostasis in mammals is primarily governed by the activities of the TRPM6 and TRPM7 cation channels, which mediate both uptake by the intestinal epithelial cells and reabsorption by the distal convoluted tubule cells in the kidney. In the nematode, C. elegans, intestinal magnesi...

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Autores principales: Teramoto, Takayuki, Sternick, Laura A., Kage-Nakadai, Eriko, Sajjadi, Shirine, Siembida, Jakub, Mitani, Shohei, Iwasaki, Kouichi, Lambie, Eric J.
Formato: Texto
Lenguaje:English
Publicado: Public Library of Science 2010
Materias:
Research Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2833210/
https://www.ncbi.nlm.nih.gov/pubmed/20221407
http://dx.doi.org/10.1371/journal.pone.0009589
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author Teramoto, Takayuki
Sternick, Laura A.
Kage-Nakadai, Eriko
Sajjadi, Shirine
Siembida, Jakub
Mitani, Shohei
Iwasaki, Kouichi
Lambie, Eric J.
author_facet Teramoto, Takayuki
Sternick, Laura A.
Kage-Nakadai, Eriko
Sajjadi, Shirine
Siembida, Jakub
Mitani, Shohei
Iwasaki, Kouichi
Lambie, Eric J.
author_sort Teramoto, Takayuki
collection PubMed
description Systemic magnesium homeostasis in mammals is primarily governed by the activities of the TRPM6 and TRPM7 cation channels, which mediate both uptake by the intestinal epithelial cells and reabsorption by the distal convoluted tubule cells in the kidney. In the nematode, C. elegans, intestinal magnesium uptake is dependent on the activities of the TRPM channel proteins, GON-2 and GTL-1. In this paper we provide evidence that another member of the TRPM protein family, GTL-2, acts within the C. elegans excretory cell to mediate the excretion of excess magnesium. Thus, the activity of GTL-2 balances the activities of the paralogous TRPM channel proteins, GON-2 and GTL-1.
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spelling pubmed-28332102010-03-11 Magnesium Excretion in C. elegans Requires the Activity of the GTL-2 TRPM Channel Teramoto, Takayuki Sternick, Laura A. Kage-Nakadai, Eriko Sajjadi, Shirine Siembida, Jakub Mitani, Shohei Iwasaki, Kouichi Lambie, Eric J. PLoS One Research Article Systemic magnesium homeostasis in mammals is primarily governed by the activities of the TRPM6 and TRPM7 cation channels, which mediate both uptake by the intestinal epithelial cells and reabsorption by the distal convoluted tubule cells in the kidney. In the nematode, C. elegans, intestinal magnesium uptake is dependent on the activities of the TRPM channel proteins, GON-2 and GTL-1. In this paper we provide evidence that another member of the TRPM protein family, GTL-2, acts within the C. elegans excretory cell to mediate the excretion of excess magnesium. Thus, the activity of GTL-2 balances the activities of the paralogous TRPM channel proteins, GON-2 and GTL-1. Public Library of Science 2010-03-08 /pmc/articles/PMC2833210/ /pubmed/20221407 http://dx.doi.org/10.1371/journal.pone.0009589 Text en Teramoto et al. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Teramoto, Takayuki
Sternick, Laura A.
Kage-Nakadai, Eriko
Sajjadi, Shirine
Siembida, Jakub
Mitani, Shohei
Iwasaki, Kouichi
Lambie, Eric J.
Magnesium Excretion in C. elegans Requires the Activity of the GTL-2 TRPM Channel
title Magnesium Excretion in C. elegans Requires the Activity of the GTL-2 TRPM Channel
title_full Magnesium Excretion in C. elegans Requires the Activity of the GTL-2 TRPM Channel
title_fullStr Magnesium Excretion in C. elegans Requires the Activity of the GTL-2 TRPM Channel
title_full_unstemmed Magnesium Excretion in C. elegans Requires the Activity of the GTL-2 TRPM Channel
title_short Magnesium Excretion in C. elegans Requires the Activity of the GTL-2 TRPM Channel
title_sort magnesium excretion in c. elegans requires the activity of the gtl-2 trpm channel
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2833210/
https://www.ncbi.nlm.nih.gov/pubmed/20221407
http://dx.doi.org/10.1371/journal.pone.0009589
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