Abstract

Of the two phosphatidylcholine biosynthetic pathways in Pyricularia oryzae, the biosynthesis of phosphatidylcholine by sequential methylations of phosphatidylethanolamine (Greenberg pathway) was inhibited by Kitazin P and edifenphos at the ED50 value for the mycelial growth of P. oryzae and the close correlation between growth inhibition and the inhibition of phosphatidylcholine biosynthesis via Greenberg pathway was observed. On the other hand, phosphatidylcholine biosynthesis from choline through CDP-choline (Kennedy pathway) was scarcely inhibited by Kitazin P and edifenphos. Phosphatidylcholine biosynthesis via the Kennedy pathway was strongly inhibited by hemicholinium-3, however, the mycelial growth was not influenced. Therefore, phosphatidylcholine biosynthesis via the Kennedy pathway was not essential for the mycelial growth of P. oryzae. No effects of Kitazin P and edifenphos on DNA, RNA, protein and chitin biosynthesis, and leakage in mycelia of P. oryzae were noted at the concentration of the ED50 value for mycelial growth. We conclude from the experimental results described that the primary antifungal action of Kitazin P and edifenphos is the inhibition of the phosphatidylcholine biosynthesis by transmethylation reaction.

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