A POSSIBLE MECHANISM OF CONTROL OF RICE BLAST DISEASE BY A NOVEL ALKOXYIMINOACETAMIDE FUNGICIDE, SSF126

When the mycelial cells of Pyricularia grisea were pulse-labeled with [S-35]-methionine in the presence of (E)-2-methoxyimino-N-methyl-2-(2- phenoxyphenyl) acetamide (SSF126), the radioactivity was time-dependen tly incorporated into a 40-kDa mitochondrial protein. The appearance o f the pulse-labeled 40-kDa protein paralleled the SSF126-dependent ind uction of cyanide-resistant respiratory activity in the mycelial cells . The SSF126-dependent induction of cyanide-resistant respiration was reversibly blocked by arbonylcyanide-p-trifluoro-methoxyphenyl-hydrazo ne (FCCP). When the mycelial cells were pulse-labeled with radioactive methionine in the presence of SSF126 and FCCP, the radioactivity was incorporated into a 41.4-kDa mitochondrial polypeptide. Upon removal o f FCCP, this polypeptide was converted into a 40-kDa protein and cyani de-resistant respiratory activity was induced in the mycelial cells. T hese findings suggested that the 41.4-kDa polypeptide is processed int o the 40-kDa mature protein responsible for the cyanide-resistant resp iration in P. grisea. Furthermore, superoxide anion (O-2(-)) was sugge sted to be involved in the SSF126-dependent induction mechanism of the cyanide-resistant respiration in the mycelial cells. Flavonoids found in plants had the ability to scavenge O-2(-) generated by blockage of electron flux through the cytochrome bc(1) segment in the mitochondri al respiratory chain and they inhibited SSF126-dependent induction of cyanide-resistant respiration. Consequently, it is feasible that SSF12 6 controls rice blast caused by P. grisea in conjunction with rice pla nt components.