Molecular and genetic characterization of ethylene involvement in mycotoxin-induced plant cell death

Abstract

AAL-toxin and the structurally related mycotoxin, fumonisin B1(FB1), cause interveinal cell death in susceptible lines of tomato with morphological characteristics of apoptosis. We observed previously that concomitant with cell death, an increase in 1-aminocyclopropane-1-carboxylic acid (ACC) and ethylene occurs, while the addition of inhibitors of ethylene biosynthesis or action significantly reduce the amount of dead tissue. Using a molecular approach, we have identified the primary ACC synthase gene family member involved, LE ACS2, and have observed an interesting aspect of its regulation. Fumonisin B1caused the accumulation of LE ACS2 mRNA with a similar time course but to a lower level than did AAL-toxin. Nevertheless, ACC levels were similar for AAL- and FB1-treated tissue. ACC oxidase mRNA was also induced by both mycotoxins, and again AAL-toxin induction was greater than that with FB1. The induction of ACC synthase and ACC oxidase mRNA observed here represents the earliest changes in gene expression noted in this cell death system to date. The effects of theNever ripemutation of tomato, which affects ethylene perception, on toxin-induced cell death also were determined. TheNever ripemutant showed significantly less necrosis or chlorosis in response to the mycotoxins than did its wild type counterpart. These results indicate that alteration in ethylene perception can markedly reduce the amount of tissue damage during this susceptible response. These findings extend our understanding of ethylene-associated signal transduction during plant cell death and suggest strategies for manipulation of cell death to enhance plant disease resistance.