Melanin biosynthesis in pyricularia oryzae site of tricyclazole inhibition and pathogenicity of melanin deficient mutants

Woloshuk, C.P.; Sisler, H.D.; Tokousbalides, M.C.; Dutky, S.R.

Pesticide Biochemistry and Physiology 14(3): 256-264

1980


ISSN/ISBN: 0048-3575
DOI: 10.1016/0048-3575(80)90032-2
Accession: 005874173

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Abstract
Tricyclazole (5-methyl-1,2,4-triazolo[3,4-b]benzothiazole) inhibited melanin synthesis in P. oryzae at concentrations 0.01 .mu.g/ml. The primary site of inhibition in the biosynthetic pathway occurred between scytalone and vermelone. Accumulation of several metabolites derived from melanin precursors along branch pathways was associated with inhibition of melanin biosynthesis. At low tricyclazole concentrations (0.01-1 .mu.g/ml), predominant accumulation of 2-hydroxyjuglone and 3,4-dihydro-3,4,8-trihydroxy-1-(2H)-naphthalenone (3,4,8-DTN) occurred as a result of the primary block between 1,3,8-trihydroxynaphthalene and vermelone. As the concentration of tricyclazole increased from 1 to 10 .mu.g/ml, flaviolin accumulation was enhanced and 3,4,8-DTN and 3,4-dihydro-4,8-dihydroxy-1-(2H) naphthalenone depressed, indicating possible secondary sites of inhibiton in the main and branch pathways. Five M-deficient mutants of P. oryzae that phenotypically resembled the tricyclazole-treated wild-type strain were nonpathogenic or rarely infected 2 rice varieties. Mutants were genetically defective in the melanin biosynthetic pathway at the site blocked by tricyclazole in the wild type. The wild-type strain converted both scytalone and vermelone to melanin; 3 mutants and the tricyclazole-treated wild type converted only vermelone to melanin. Data suggested a relationship between melanin biosynthesis and pathogenicity in P. oryzae.