STRESS SIGNALING THROUGH CA2+ CALMODULIN-DEPENDENT PROTEIN PHOSPHATASE CALCINEURIN MEDIATES SALT ADAPTATION IN PLANTS/

Citation
Jm. Pardo et al., STRESS SIGNALING THROUGH CA2+ CALMODULIN-DEPENDENT PROTEIN PHOSPHATASE CALCINEURIN MEDIATES SALT ADAPTATION IN PLANTS/, Proceedings of the National Academy of Sciences of the United Statesof America, 95(16), 1998, pp. 9681-9686
Citations number
28
Categorie Soggetti
Multidisciplinary Sciences
ISSN journal
00278424
Volume
95
Issue
16
Year of publication
1998
Pages
9681 - 9686
Database
ISI
SICI code
0027-8424(1998)95:16<9681:SSTCCP>2.0.ZU;2-C
Abstract
Calcineurin (CaN) is a Ca2+- and calmodulin-dependent protein phosphat ase (PP2B) that, in yeast, is an integral intermediate of a salt-stres s 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 t ransgenic tobacco plants to reconstitute a constitutively activated ph osphatase in vivo, Several different transgenic lines that expressed a ctivated CaN also exhibited substantial NaCl tolerance, and this trait was linked to the genetic inheritance of the CaN transgene, Enhanced capacity of plants expressing CaN to survive NaCl shock was similar wh en evaluation was conducted on seedlings in tissue culture raft vessel s or plants in hydroponic culture that were transpiring actively, Root growth was less perturbed than shoot growth by NaCl in plants express ing CaN, Also, NaCl stress survival of control shoots was enhanced sub stantially when grafted onto roots of plants expressing CaN, further i mplicating a significant function of the phosphatase in the preservati on of root integrity during salt shock. Together, these results indica te 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 expressi on of an activated regulatory intermediate substantially enhanced salt tolerance.