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Bad Homburg vor der Höhe, Germany

Georgiev P.,Babraham Institute | Georgiev P.,Max Planck Institute of Immunobiology | Okkenhaug H.,Babraham Institute | Drews A.,Emmy Noether Research Group | And 8 more authors.
Cell Metabolism | Year: 2010

TRPM channels have emerged as key mediators of diverse physiological functions. However, the ionic permeability relevant to physiological function in vivo remains unclear for most members. We report that the single Drosophila TRPM gene (dTRPM) generates a conductance permeable to divalent cations, especially Zn2+ and in vivo a loss-of-function mutation in dTRPM disrupts intracellular Zn2+ homeostasis. TRPM deficiency leads to profound reduction in larval growth resulting from a decrease in cell size and associated defects in mitochondrial structure and function. These phenotypes are cell-autonomous and can be recapitulated in wild-type animals by Zn 2+ depletion. Both the cell size and mitochondrial defect can be rescued by extracellular Zn2+ supplementation. Thus our results implicate TRPM channels in the regulation of cellular Zn2+ in vivo. We propose that regulation of Zn2+ homeostasis through dTRPM channels is required to support molecular processes that mediate class I PI3K-regulated cell growth. © 2010 Elsevier Inc.

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