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Open Access item An osmotically induced cytosolic Ca2+ transient activates calcineurin signaling to mediate ion homeostasis and salt tolerance of saccharomyces cerevisiae

Authors:Matsumoto, Tracie
Ellsmore, Amanda J.
Cessna, Stephen G.
Low, Phillip S.
Pardo, José M.
Bressan, Ray A.
Hasegawa, Paul M.
Issue Date:Sep-2002
Publisher:American Society for Biochemistry and Molecular Biology
Citation:Journal of Biological Chemistry 277 (36): 33075-33080 (2002).
Abstract:Hyperosmotic stress caused by NaCl, LiCl, or sorbitol induces an immediate and short duration (∼1 min) transient cytosolic Ca2+([Ca2+]cyt) increase (Ca2+-dependent aequorin luminescence) inSaccharomyces cerevisiae cells. The amplitude of the osmotically induced [Ca2+]cyttransient was attenuated by the addition of chelating agents EGTA or BAPTA, cation channel pore blockers, competitive inhibitors of Ca2+ transport, or mutations (cch1Δ ormid1Δ) that reduce Ca2+ influx, indicating that Ca Formula is a source for the transient. An osmotic pretreatment (30 min) administered by inoculating cells into media supplemented with either NaCl (0.4 or 0.5 m) or sorbitol (0.8 or 1.0 m) enhanced the subsequent growth of these cells in media containing 1 m NaCl or 2 msorbitol. Inclusion of EGTA in the osmotic pretreatment media or the cch1Δ mutation reduced cellular capacity for NaCl but not hyperosmotic adaptation. The stress-adaptive effect of hyperosmotic pretreatment was mimicked by exposing cells briefly to 20 mm CaCl2. Thus, NaCl- or sorbitol-induced hyperosmotic shock causes a [Ca2+]cyt transient that is facilitated by Ca2+ influx, which enhances ionic but not osmotic stress adaptation. NaCl-induced ENA1expression was inhibited by EGTA, cch1Δ mutation, and FK506, indicating that the [Ca2+]cyt transient activates calcineurin signaling to mediate ion homeostasis and salt tolerance.
Description:6 pages, 5 figures, 71 references.
Publisher version (URL):DOI 10.1074/jbc.M205037200
http://www.jbc.org/content/277/36/33075.full
URI:http://hdl.handle.net/10261/37948
ISSN:0021-9258
Appears in Collections:(IRNAS) Artículos

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