Metal ions suppress the abnormal taste behavior of the Drosophila mutant malvolio.

Abstract

A mutation in the malvolio (mvl) gene affects taste behavior in Drosophila melanogaster. The malvolio gene encodes a protein (MVL) that exhibits homology to the mammalian natural resistance-associated macrophage proteins. It is also homologous to the Smf1 protein from Saccharomyces cerevisiae, which we have recently demonstrated to function as a Mn2+/Zn2+ transporter. We proposed that the Drosophila and mammalian proteins, like the yeast SMF1 gene product, are metal-ion transporters. To test this hypothesis, malvolio mutant flies were allowed to develop, from egg to adulthood, on a medium containing elevated concentrations of metal ions. Mutant flies that were reared in the presence of 10 mmol l-1 MnCl2 or FeCl2 developed into adults with recovered taste behavior. CaCl2 or MgCl2 had no effect on the mutant's taste perception. ZnCl2 inhibited the effect of MnCl2 when both ions were supplied together. Similar suppression of the abnormal taste behavior was observed when mvl mutants were fed MnCl2 or FeCl2 only at the adult stage. Furthermore, exposure of adult mutant flies to these ions in the testing plate for only 2 h was sufficient to restore normal taste behavior. The suppression of the defective taste behavior suggests that MVL functions as a Mn2+/Fe2+ transporter and that Mn2+ and/or Fe2+ are involved in the signal transduction of taste perception in Drosophila adults.