English
 
User Manual Privacy Policy Disclaimer Contact us
  Advanced SearchBrowse

Item

ITEM ACTIONS
  This item is discarded!DetailsSummary

Discarded

Journal Article

TRPM channels mediate zinc homeostasis and cellular growth during Drosophila larval development

MPS-Authors
/persons/resource/persons182731

Flick,  M.
Department of Molecular Sensory Systems, Center of Advanced European Studies and Research (caesar), Max Planck Society;

External Ressource

(No access)

(No access)

Fulltext (public)
There are no public fulltexts stored in PuRe
Supplementary Material (public)
There is no public supplementary material available
Citation

Georgiev, P., Okkenhaug, H., Drews, A., Wright, D., Lambert, S., Flick, M., et al. (2010). TRPM channels mediate zinc homeostasis and cellular growth during Drosophila larval development. Cell Metabolism, 12(4), 386-397. doi:S1550-4131(10)00298-6 [pii];10.1016/j.cmet.2010.08.012 [doi].


Abstract
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 Zn(2+) and in vivo a loss-of-function mutation in dTRPM disrupts intracellular Zn(2+) 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 Zn(2+) supplementation. Thus our results implicate TRPM channels in the regulation of cellular Zn(2+) in vivo. We propose that regulation of Zn(2+) homeostasis through dTRPM channels is required to support molecular processes that mediate class I PI3K-regulated cell growth