SYSTEMIN POTENTIATES THE OXIDATIVE BURST IN CULTURED TOMATO CELLS

Plants that have been wounded by insects or other herbivores may be mo re susceptible to infection by adventitious microbes. Wound-induced si gnal molecules, which serve to induce responses in the plant that reta rd further feeding, might also act to prepare a plant for possible pat hogen attack. We have examined the effect of a wound-generated systemi c messenger (systemin) on a pathogen-stimulated defense-response marke r, the oxidative burst. We observed that neither systemin nor its inac tive analog (A-17) was able to directly induce H2O2 biosynthesis in su spension-cultured tomato (Lycopersicon esculentum L.) cells, regardles s of the duration of exposure of the cells to the two peptides. Simila rly, neither systemin nor A-17 was capable of modifying an oligogalact uronide-elicited oxidative burst, as long as elicitor addition occurre d within minutes of treatment with systemin or A-17. In contrast, pree xposure of the cell cultures to systemin (but not to A-17) led to a ti me-dependent enhancement of the oligogalacturonide-elicited oxidative burst. By 12 h of exposure, the H2O2 biosynthetic capacity of systemin -treated cells exceeded that of the control cells by a factor of 16 +/ - 2. A similar up-regulation by systemin of a mechanically stimulated oxidative burst was also observed. Because the systemin-induced augmen tation in oxidant synthesis is quantitatively prevented by coincubatio n with 2 mu M cycloheximide, and because the oxidative burst of oligog alacturonic acid-elicited control cells (no systemin exposure) is unaf fected by preincubation with cycloheximide, we conclude that systemin enhancement of the tomato-cell oxidative burst requires protein synthe sis.