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

FEBS Lett. 2011 Jul 21;585(14):2275-8. doi: 10.1016/j.febslet.2011.05.052. Epub 2011 May 27.

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+).

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Cation Transport Proteins / genetics
  • Cation Transport Proteins / metabolism*
  • Cell Line
  • Chickens
  • Gene Expression Regulation
  • Gene Knockdown Techniques
  • Humans
  • Magnesium / metabolism*
  • Protein-Serine-Threonine Kinases
  • TRPM Cation Channels / genetics
  • TRPM Cation Channels / metabolism*

Substances

  • Cation Transport Proteins
  • MagT1 protein, human
  • TRPM Cation Channels
  • Protein-Serine-Threonine Kinases
  • TRPM7 protein, human
  • Magnesium