Reference Report

Reference
Citation	Hofmann, T., Chubanov, V., Chen, X., Dietz, A.S., Gudermann, T., Montell, C. (2010). Drosophila TRPM channel is essential for the control of extracellular magnesium levels. PLoS ONE 5(5): e10519. (Export to RIS)
FlyBase ID	FBrf0210792
Publication Type	Research paper
PubMed ID	20463899
PubMed Abstract	The TRPM group of cation channels plays diverse roles ranging from sensory signaling to Mg2+ homeostasis. In most metazoan organisms the TRPM subfamily is comprised of multiple members, including eight in humans. However, the Drosophila TRPM subfamily is unusual in that it consists of a single member. Currently, the functional requirements for this channel have not been reported. Here, we found that the Drosophila TRPM protein was expressed in the fly counterpart of mammalian kidneys, the Malpighian tubules, which function in the removal of electrolytes and toxic components from the hemolymph. We generated mutations in trpm and found that this resulted in shortening of the Malpighian tubules. In contrast to all other Drosophila trp mutations, loss of trpm was essential for viability, as trpm mutations resulted in pupal lethality. Supplementation of the diet with a high concentration of Mg2+ exacerbated the phenotype, resulting in growth arrest during the larval period. Feeding high Mg2+ also resulted in elevated Mg2+ in the hemolymph, but had relatively little effect on cellular Mg2+. We conclude that loss of Drosophila trpm leads to hypermagnesemia due to a defect in removal of Mg2+ from the hemolymph. These data provide the first evidence for a role for a Drosophila TRP channel in Mg2+ homeostasis, and underscore a broad and evolutionarily conserved role for TRPM channels in Mg2+ homeostasis.
DOI	10.1371/journal.pone.0010519
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Language of Publication	English
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Publication Type	Journal
Abbreviation	PLoS ONE
Title	PLoS ONE
Publication Year	2006-
ISBN/ISSN	1932-6203
Data from Reference
Aberrations (1)
	Df(2R)XTE-18
Alleles (5)
	trpm¹ trpm^{2.Scer\SceI.RS} trpm² trpm^EY01618 w^+mW.hs
Constructs (1)
	P{FRT(trpm.2.Scer\SceI.RS)}
Genes (1)
	trpm
Insertions (1)
	P{EPgy2}trpm^EY01618
Natural transposons (1)
	P-element