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Published 7 January 2002. doi:10.1083/jcb.200111004
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© The Rockefeller University Press, 0021-9525/2002/1/29 $5.00
The Journal of Cell Biology, Volume 156, Number 1, January 7, 2002 29-34

Report

Internal Ca2+ release in yeast is triggered by hypertonic shock and mediated by a TRP channel homologue



Valérie Denis and Martha S. Cyert

Department of Biological Sciences, Stanford University, Stanford, CA 94305

Address correspondence to Martha S. Cyert, Dept. of Biological Sciences, 208B Gilbert Bldg., Stanford University, Stanford, CA 94305-5020. Tel.: (650) 723-9970. Fax: (650) 725-8309. E-mail: mcyert{at}leland.stanford.edu

Calcium ions, present inside all eukaryotic cells, are important second messengers in the transduction of biological signals. In mammalian cells, the release of Ca2+ from intracellular compartments is required for signaling and involves the regulated opening of ryanodine and inositol-1,4,5-trisphosphate (IP3) receptors. However, in budding yeast, no signaling pathway has been shown to involve Ca2+ release from internal stores, and no homologues of ryanodine or IP3 receptors exist in the genome. Here we show that hyperosmotic shock provokes a transient increase in cytosolic Ca2+ in vivo. Vacuolar Ca2+, which is the major intracellular Ca2+ store in yeast, is required for this response, whereas extracellular Ca2+ is not. We aimed to identify the channel responsible for this regulated vacuolar Ca2+ release. Here we report that Yvc1p, a vacuolar membrane protein with homology to transient receptor potential (TRP) channels, mediates the hyperosmolarity induced Ca2+ release. After this release, low cytosolic Ca2+ is restored and vacuolar Ca2+ is replenished through the activity of Vcx1p, a Ca2+/H+ exchanger. These studies reveal a novel mechanism of internal Ca2+ release and establish a new function for TRP channels.

Key Words: calcium signaling; ion channels; osmotic pressure; vacuoles; Saccharomyces cerevisiae


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