Reference: Zhou H and Clapham DE (2009) Mammalian MagT1 and TUSC3 are required for cellular magnesium uptake and vertebrate embryonic development. Proc Natl Acad Sci U S A 106(37):15750-5

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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.

Reference Type
Journal Article | Research Support, Non-U.S. Gov't
Authors
Zhou H, Clapham DE
Primary Lit For
ALR1

Disease Annotations


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Gene Disease Ontology Term Qualifier Evidence Method Source Assigned On Reference

Functional Complementation Annotations 2 entries for 2 complements


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GeneSpeciesGene IDStrain backgroundDirectionDetailsSource
ALR1Homo sapiensHGNC:28880S288Cother complements yeastHuman MAGT1 does not have sequence similarity to yeast ALR1 but functionally complements the magnesium transport defect of the alr1 mutant.SGD
ALR1Homo sapiensHGNC:30242S288Cother complements yeastHuman TUSC3 does not have sequence similarity to yeast ALR1 but functionally complements the magnesium transport defect of the alr1 mutant. Isoform 2 (UniProt Q13454-2) complements the yeast mutation but isoform 1 does not.SGD
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