The Mg2+ transporter MagT1 partially rescues cell growth and Mg2+ uptake in cells lacking the channel-kinase TRPM7

University of Colorado, Denver, Colorado, United States
FEBS letters (Impact Factor: 3.34). 05/2011; 585(14):2275-8. DOI: 10.1016/j.febslet.2011.05.052
Source: PubMed

ABSTRACT Magnesium (Mg(2+)) transport across membranes plays an essential role in cellular growth and survival. TRPM7 is the unique fusion of a Mg(2+) permeable pore with an active cytosolic kinase domain, and is considered a master regulator of cellular Mg(2+) homeostasis. We previously found that the genetic deletion of TRPM7 in DT40 B cells results in Mg(2+) deficiency and severe growth impairment, which can be rescued by supplementation with excess extracellular Mg(2+). Here, we show that gene expression of the Mg(2+) selective transporter MagT1 is upregulated in TRPM7(-/-) cells. Furthermore, overexpression of MagT1 in TRPM7(-/-) cells augments their capacity to uptake Mg(2+), and improves their growth behavior in the absence of excess Mg(2+).

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Available from: Anne-Laure Perraud, Jul 28, 2015
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    • "The view that TRPM7 plays a role in maintaining cellular Mg 2+ homeostasis mainly centers on the observation that TRPM7- deficiency leads to reduced [Mg 2+ ] i in a number of cell types (Abed and Moreau, 2009; Chen et al., 2012; He et al., 2005; Rybarczyk et al., 2012; Zhang et al., 2011). In addition, defects in cell growth, cytoskeletal organization or migration due to TRPM7-deficiency in cultured cells, embryonic stem cells and Xenopus embryos, were largely rescued by either Mg 2+ supplementation (to supraphysiological levels) or by expression of the Mg 2+ -transporters SLC41A2 or MagT1 (Abed and Moreau, 2009; Callera et al., 2009; Deason-Towne et al., 2011; Liu et al., 2011; Ryazanova et al., 2010; Rybarczyk et al., 2012; Schmitz et al., 2003; Su et al., 2011). In contrast, studies by the Clapham lab indicate that TRPM7 is not critically required for cellular Mg 2+ homeostasis. "
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