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Proc Natl Acad Sci U S A. 2009 Sep 15;106(37):15750-5. doi: 10.1073/pnas.0908332106. Epub 2009 Aug 26.

Mammalian MagT1 and TUSC3 are required for cellular magnesium uptake and vertebrate embryonic development.

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1
Department of Cardiology, Howard Hughes Medical Institute, Manton Center for Orphan Disease, Children's Hospital Boston, and Harvard Medical School, 1309 Enders, 320 Longwood Avenue, Boston, MA 02115, USA.

Abstract

Magnesium (Mg(2+)) is the second most abundant cation in cells, yet relatively few mechanisms have been identified that regulate cellular levels of this ion. The most clearly identified Mg(2+) transporters are in bacteria and yeast. Here, we use a yeast complementary screen to identify two mammalian genes, MagT1 and TUSC3, as major mechanisms of Mg(2+) influx. MagT1 is universally expressed in all human tissues and its expression level is up-regulated in low extracellular Mg(2+). Knockdown of either MagT1 or TUSC3 protein significantly lowers the total and free intracellular Mg(2+) concentrations in mammalian cell lines. Morpholino knockdown of MagT1 and TUSC3 protein expression in zebrafish embryos results in early developmental arrest; excess Mg(2+) or supplementation with mammalian mRNAs can rescue the effects. We conclude that MagT1 and TUSC3 are indispensable members of the vertebrate plasma membrane Mg(2+) transport system.

PMID:
19717468
PMCID:
PMC2732712
DOI:
10.1073/pnas.0908332106
[Indexed for MEDLINE]
Free PMC Article

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