1999 Volume 24 Issue 4 Pages 369-374
Carpropamid {(1RS, 3SR)-2, 2-dichloro-N-[1-(4-chlorophenyl) ethyl]-1-ethyl-3-methyl cyclopropanecarboxamide}, which is considered as a melanin biosynthesis inhibitor, enhanced the accumulation of the phytoalexins momilactone A and sakuranetin in the rice leaves subsequently inoculated with the blast pathogen (Pyricularia oryzae). Carpropamid and its two diastereo-isomers, A(1R, 3S) and B(1S, 3R), did not stimulate phytoalexin production directly, but they potentiated rice plants to produce the two phytoalexins more rapidly and much amounts in response to blast infection. This phenomenon was also observed in rice leaves treated with WL28325 (2, 2-dichloro-3, 3-dimethylcyclopropane carboxylic acid), a resistance inducer. The calculation data of the correlation among accumulation of phytoalexins, concentrations of chemicals and biological effects suggested that the correlation pattern of isomer A resembled that of WL28325. The main mode of action of isomer A appears to be an enhancement of phytoalexin synthesis during blast infection (EPAS mode) similar to that of WL28325, rather than the inhibition of melanin biosynthesis (MBI mode). In contrast, the main mode of action of isomer B was found to be MBI, although EPAS probably also contributes to its biological activity. Carpropamid is assumed to control rice blast through a combination of MBI and EPAS activities.
