| Summary: | Transient potential receptor (TRP) channels are conserved cation channels found in most eukaryotes, known to sense a variety of chemical, thermal or mechanical stimuli. The <i>Saccharomyces cerevisiae</i> TRPY1 is a TRP channel with vacuolar localization involved in the cellular response to hyperosmotic shock and oxidative stress. In this study, we found that <i>S. cerevisiae</i> diploid cells with heterozygous deletion in <i>TRPY1</i> gene are haploinsufficient when grown in synthetic media deficient in essential metal ions and that this growth defect is alleviated by non-toxic Mn<sup>2+</sup> surplus. Using cells expressing the Ca<sup>2+</sup>-sensitive photoprotein aequorin we found that Mn<sup>2+</sup> augmented the Ca<sup>2+</sup> flux into the cytosol under oxidative stress, but not under hyperosmotic shock, a trait that was absent in the diploid cells with homozygous deletion of <i>TRPY1</i> gene. TRPY1 activation under oxidative stress was diminished in cells devoid of Smf1 (the Mn<sup>2+</sup>-high-affinity plasma membrane transporter) but it was clearly augmented in cells lacking Pmr1 (the endoplasmic reticulum (ER)/Golgi located ATPase responsible for Mn<sup>2+</sup> detoxification via excretory pathway). Taken together, these observations lead to the conclusion that increased levels of intracytosolic Mn<sup>2+</sup> activate TRPY1 in the response to oxidative stress.
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