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

AAL-toxin and the structurally related mycotoxin, fumonisin B-1 (FB1), caus e 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 i nvolved, LE ACS2, and have observed an interesting aspect of its regulation . Fumonisin B-1 caused the accumulation of LE ACS2 mRNA with a similar time course but to a lower level than did AAL-toxin. Nevertheless, ACC levels w ere similar for AAL- and FB1-treated tissue. ACC oxidase mRNA was also indu ced by both mycotoxins, and again AAL-toxin induction was greater than that with FB,. The induction of ACC synthase and ACC oxidase mRNA observed here represents the earliest changes in gene expression noted in this cell deat h system to date. The effects of the Never ripe mutation of tomato, which a ffects ethylene perception, on toxin-induced cell death also were determine d. The Never ripe mutant showed significantly less necrosis or chlorosis in response to the mycotoxins than did its wild type counterpart. These resul ts indicate that alteration in ethylene perception can markedly reduce the amount of tissue damage during this susceptible response. These findings ex tend our understanding of ethylene-associated signal transduction during pl ant cell death and suggest strategies for manipulation of cell death to enh ance plant disease resistance. (C) 1999 Academic Press.