Genetic Analysis of Melanin-Deficient, Nonpathogenic Mutants of Magnaporthe grisea. Forrest G. Chumley. Central Research and Development Department, E. I. du Pont de Nemours and Co., Inc., Wilmington, DE 19880-0402 U.S.A. Barbara Valent. Central Research and Development Department, E. I. du Pont de Nemours and Co., Inc., Wilmington, DE 19880-0402 U.S.A. MPMI 3:135-143. Accepted 13 November 1989. Copyright 1990 The American Phytopathological Society.

The fungus Magnaporthe grisea causes rice blast disease and gray leaf spot disease of other grasses. Numerous M. grisea mutants that fail to produce the dark gray pigment typical of wild-type mycelia have been isolated and analyzed. Three classes of mutants have been distinguished based on pigmentation phenotypes: albino (Alb^–), rosy (Rsy^–), and buff (Buf^–). Some pigment mutants were recovered following mutagenesis, and others appeared spontaneously. Spontaneous Buf^– mutants have been particularly common. Genetic analysis has shown that the three mutant phenotypes are due to single gene defects at unlinked loci. Genetic crosses have yielded the three possible classes of double mutants. Analysis of the double mutants has revealed epistasis relationships: alb^{– rsy–} and alb^– buf^– mutants are Alb^–, whereas rsy^– buf^– mutants are Rsy^–. These epistasis relationships are consistent with the order of function ALB⁺ ‾RSY⁺ ‾ BUF⁺ in melanin biosynthesis. All the pigment mutants tested failed to infect intact host plants, but the same mutants successfully infected plants that had been wounded by abrading the leaf epidermis. When scytalone, an intermediate in the biosynthetic pathway leading to dihydroxynaphthalene-based fungal melanins, was added to the growth medium, petri plate cultures of alb^– mutants, but not rsy^– or buf^– mutants, darkened noticeably. When scytalone was incorporated in spore suspensions sprayed onto unwounded host plants, pathogenicity was restored to alb^–, but not to rsy^– or buf^– mutants.