AAL-TOXIN INDUCED PHYSIOLOGICAL-CHANGES IN LYCOPERSICON-ESCULENTUM MILL - ROLES FOR ETHYLENE AND PYRIMIDINE INTERMEDIATES IN NECROSIS

Treatment off, near-isogenic asc/asc tomato leaflets with Alternaria a lternata f.sp. lycopersici (AAL)-toxin (0.015 mu m) increased steady s tate levels of 1-aminocydopropane-1-carboxylic acid (ACC) after 6 h, f ollowed by ethylene evolution after 12 h, followed by the detection of necrosis after 36 h. No changes in these parameters were detected in comparably treated leaflets of the Asc/Asc isoline or water controls. Co-treatment of asc/asc leaflets with AAL-toxin and ethylene inhibitor s, aminoethoxyvinylglycine or silver thiosulphate, markedly reduced ne crosis and ethylene evolution. Application of exogenous ACC (1 mM) in the presence of AAL-toxin resulted in a two-fold increase in ethylene evolution and interveinal necrosis. However, no necrosis resulted when 1 mM ACC enhanced ethylene levels to 108 nl g(-1) h(-1) in control ti ssues without AAL-toxin, even though the ethylene level was similar to that induced by AAL-toxin. Dihydroorotic acid, an intermediate in pyr imidine biosynthesis, at 0.3 mu M abolished both the AAL-toxin increas e in ACC and necrosis. Addition of N-(phosphonacetyl)-L-aspartate, a s pecific inhibitor of pyrimidine biosynthesis, elicited interveinal nec rosis resembling AAL-toxin treatment. These results indicate an integr al but not causal role for ethylene in AAL-toxin-induced necrosis and suggest a metabolic interaction involving a negative regulation of the erotic acid on the ethylene biosynthetic pathways.