Submitted to: Plant Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/15/2003
Publication Date: 8/31/2003
Citation: DOMBROWSKI, J.E. SALT STRESS ACTIVATION OF WOUND-RELATED GENES IN TOMATO PLANTS. PLANT PHYSIOLOGY. 2003. v. 132(4). p. 2098-2107. Interpretive Summary: Plants in the field are exposed to multiple stresses, and their response to these various stresses determines their capacity to survive. Tomato plants respond to mechanical wounding or herbivorous insect attack by inducing the synthesis of a wide array of defense related proteins. We have found water deficit stress (wilting and salt stress) caused the accumulation defense proteins in tomato plants and made them more responsive to wounding. The activation of these wound response proteins by water deficit stress could protect the plant against defoliating chewing insects during periods of low growth and preserve limited foliage until water resources are no longer limiting, thereby improving their survivability.
Technical Abstract: 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 caused the accumulation of proteinase inhibitors and the activation of other wound-related genes in tomato plants. Salt stress was also found to enhance the plant's response to wounding both 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 JA-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 accumulation of proteinase inhibitors, but was necessary to achieve maximal levels. These results suggest that a prosystemin independent but JA-dependent pathway is utilized for proteinase inhibitor accumulation in response to salt stress.