Reference: Zhou H and Clapham DE (2009)
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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
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Journal Article |
Research Support, Non-U.S. Gov't
- Authors
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Zhou H,
Clapham DE
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- ALR1
Gene Ontology Annotations
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Gene | Species | Gene ID | Strain background | Direction | Details | Source |
ALR1 | Homo sapiens | HGNC:28880 | S288C | other complements yeast | Human MAGT1 does not have sequence similarity to yeast ALR1 but functionally complements the magnesium transport defect of the alr1 mutant. | SGD |
ALR1 | Homo sapiens | HGNC:30242 | S288C | other complements yeast | Human 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 |