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.
journal_name
Cell Metabjournal_title
Cell metabolismauthors
Georgiev P,Okkenhaug H,Drews A,Wright D,Lambert S,Flick M,Carta V,Martel C,Oberwinkler J,Raghu Pdoi
10.1016/j.cmet.2010.08.012subject
Has Abstractpub_date
2010-10-06 00:00:00pages
386-397issue
4eissn
1550-4131issn
1932-7420pii
S1550-4131(10)00298-6journal_volume
12pub_type
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