Target site of a new antifungal compound KC10017 in the melanin biosynthesis of Magnaporthe grisea

• Published in: Pesticide biochemistry and physiology 1998-11, Vol.62 (2), p.102-112
• Main Authors: Kim, J.C, Min, J.Y, Kim, H.T, Kim, B.S, Kim, Y.S, Kim, B.T, Yu, S.H, Yamaguchi, I, Cho, K.Y
• Format: Article
• Language: English
• Subjects: biochemical pathways; Biological and medical sciences; biosynthesis; Chemical control; Control; Fundamental and applied biological sciences. Psychology; Fungal plant pathogens; fungicides; growth; inhibition; KC-10017; Magnaporthe grisea; mechanism of action; melanins; Oryza sativa; Phytopathology. Animal pests. Plant and forest protection; plant pathogenic fungi; spore germination
• ISSN: 0048-3575; 1095-9939
• DOI: 10.1006/pest.1998.2377

A new experimental fungicide KC10017 (3-[4'-bromo-2',6'-dimethylphenoxy]methyl-4 [(3"-methylphenyl) aminocarbonyl]methyl-1,2,4-oxadiazol-5-one) completely controlled rice blast disease at more than 1.0 micrograms/ml without curative activity. When the chemical was applied after the inoculation was made with injury, the fungicide had no effect on controlling rice blast. The fungicide at concentrations of more than 1 microgram/ml blocked appressorial melanization and penetration of cellophane membrane by Magnaporthe grisea P-2 without affecting fungal growth, spore germination, and appressorial formation. To elucidate the target site of KC10017 in melanin biosynthesis inhibition, M. grisea P-2 was grown in potato dextrose broths treated with both KC10017 and tricyclazole. The mycelia and culture media of cultures treated with both KC10017 and tricyclazole at a concentration of 5 micrograms/ml each became colorless like as the cultures treated with KC10017 alone, whereas the tricyclazole-treated cultures exhibited red color. Shunt products of 3,4-dihydro-3,4,8-trihydroxy- 1-(2H)-naphthalenone, 3,4-dihydro-4,8-dihydroxy- 1-(2H)-naphthalenone, 3,4-dihydro-4,6,8-trihydroxy-1-(2H)-naphthalenone, and 4-hydroxyscytalone were absent or present in only trace amounts in the cultures treated with KC10017 alone or both KC10017 and tricyclazole. However, they were detected at much higher levels in the cultures treated with tricyclazole alone. On the other hand, appressorial melanization and penetration ability in M. grisea treated with KC10017 was recovered by the addition of scytalone. These results demonstrate that the target site of KC10017 in melanin biosynthesis inhibition is at the pentaketide synthesis step and/or at the pentaketide cyclization step prior to 1,3,6,8-tetrahydroxynaphthalene formation.