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Stress Signaling Through Ca2+/Calmodulin-Dependent Protein Phosphatase Calcineurin Mediates Salt Adaptation in Plants

Jose M. Pardo, Muppala P. Reddy, Shuli Yang, Albino Maggio, Gyung-Hye Huh, Tracie Matsumoto, Maria A. Coca, Matilde Paino-D'Urzo, Hisashi Koiwa, Dae-Jin Yun, Abed A. Watad, Ray A. Bressan and Paul M. Hasegawa
Proceedings of the National Academy of Sciences of the United States of America
Vol. 95, No. 16 (Aug. 4, 1998), pp. 9681-9686
Stable URL: http://www.jstor.org/stable/45535
Page Count: 6
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Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Stress Signaling Through Ca2+/Calmodulin-Dependent Protein Phosphatase Calcineurin Mediates Salt Adaptation in Plants
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Abstract

Calcineurin (CaN) is a Ca2+- and calmodulin-dependent protein phosphatase (PP2B) that, in yeast, is an integral intermediate of a salt-stress signal transduction pathway that effects NaCl tolerance through the regulation of Na+ influx and efflux. A truncated form of the catalytic subunit and the regulatory subunit of yeast CaN were coexpressed in transgenic tobacco plants to reconstitute a constitutively activated phosphatase in vivo. Several different transgenic lines that expressed activated CaN also exhibited substantial NaCl tolerance, and this trait was linked to the genetic inheritance of the CaN transgenes. Enhanced capacity of plants expressing CaN to survive NaCl shock was similar when evaluation was conducted on seedlings in tissue culture raft vessels or plants in hydroponic culture that were transpiring actively. Root growth was less perturbed than shoot growth by NaCl in plants expressing CaN. Also, NaCl stress survival of control shoots was enhanced substantially when grafted onto roots of plants expressing CaN, further implicating a significant function of the phosphatase in the preservation of root integrity during salt shock. Together, these results indicate that in plants, like in yeast, a Ca2+- and calmodulin-dependent CaN signal pathway regulates determinants of salt tolerance required for stress adaptation. Furthermore, modulation of this pathway by expression of an activated regulatory intermediate substantially enhanced salt tolerance.

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