Magnesium excretion in C. elegans requires the activity of the GTL-2 TRPM channel.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 20221407.
- Also identified by DOI 10.1371/journal.pone.0009589 and PMC identifier 2833210.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
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.
Medical subject headings
- Caenorhabditis elegans
- Caenorhabditis elegans Proteins
- Ion Channels
- Magnesium
- TRPM Cation Channels