First published online July 10, 2003; 10.1104/pp.102.019927
Plant Physiology 132:2098-2107 (2003)
© 2003 American Society of Plant Biologists
CELL BIOLOGY AND SIGNAL TRANSDUCTION
Salt Stress Activation of Wound-Related Genes in Tomato Plants1
James E. Dombrowski*
U.S. Department of Agriculture-Agricultural Research Service, National
Forage Seed Production Research Center, Oregon State University, Corvallis,
Oregon 97331–7102
Plants respond to various stresses by expressing distinct sets of genes.
The effects of multiple stresses on plants and their interactions are not well
understood. We have discovered that salt stress causes the accumulation of
proteinase inhibitors and the activation of other wound-related genes in
tomato (Lycopersicon esculentum) plants. Salt stress was also found
to enhance the plant's response to wounding locally and systemically. The
tomato mutant (def-1), which has an impairment in the octadecanoid
pathway, displayed a severe reduction in the accumulation of proteinase
inhibitors under salt stress, indicating that salt stress-induced accumulation
of proteinase inhibitors was jasmonic acid dependent. The analysis of salt
stress in another tomato mutant, spr-1, which carries a mutation in a
systemin-specific signaling component, and transgenic tomato plants that
express an antisense-prosystemin cDNA, showed that prosystemin
activity was not required for the salt-induced accumulation of proteinase
inhibitors, but was necessary to achieve maximal levels. These results suggest
that a prosystemin independent- but jasmonic acid-dependent pathway is
utilized for proteinase inhibitor accumulation in response to salt stress.
1 This research was supported in part by Washington State University College
of Agriculture and Home Economics (Project no. 1791), by the National Science
Foundation (grant no. IBN 9601099), and by the U.S. Department of
Agriculture/Competitive Grants Research Office (grant no. WNP03153).
*
E-mail
dombrowj{at}onid.orst.edu;
fax 541–738–4160.
Received December 31, 2002;
returned for revision February 25, 2003;
accepted April 29, 2003.
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