Yasuo Kawase

Selective Inhibition of the Demethylation at C-14 in Ergosterol Biosynthesis by the Fungicide, Denmert (S-1358)

In cell-free homogenates of Saccharomyces cerevisiae, Denmert (S-1358) inhibited the incorporation of radioactivity from dl-mevalonate-2-14C into 14-desmethyl-lanosterol, 4α-methyl-cholesta-8,24-dien-3-one, 4α-methyl-zymosterol and 4-desmethyl sterols (zymosterol and episterol) at a concentration of 10−4 m. Concomitantly, a large accumulation of radioactivity was observed in the Ianosterol fraction.In good agreement with the results described above, Denmert inhibited the conversion of 14C-labeled lanosterol to 4-desmethyl sterols, while the conversion of 14C-labeled 14-desmethyl-lanosterol to 4-desmethyl sterols was hardly affected by the fungicide. It is therefore evident that Denmert is a potent selective inhibitor of the demethylation at the C–14 position in ergosterol biosynthesis.The fungicide, triarimol, was also found to exhibit the same effect on sterol biosynthesis as Denmert.

Systemic movement in cucumber plants and control of cucumber gray mould by a new fungicide, S-7131

Carbon-14-labelled S-7131 (N-(3′,5′-dichlorophenyl)-1,2-dimethylcyclopropane-1,2-dicarboximide) penetrated into the treated leaves of cucumber plants, moved to the stem and was then translocated both upwards and slightly downwards. Also through roots the fungicide was readily taken up and translocated to aerial parts. Autoradiographs showed that S-7131 had a tendency to accumulate at the leaf margin. In experiments with cucumber plants bearing flowers and fruits it was shown that S-7131 hardly moved from foliage to flowers and fruits. TLC analysis of radioactive extracts showed that S-7131 moved within plants in the unaltered form. Bioassay tests confirmed that systemic movement of S-7131 contributed to its high efficacy in disease control.

Nature of Procymidone-Tolerant Botrytis Cinerea Strains Obtained in Vitro

Tolerance of plant pathogens to fungicides was not a serious problem when mainly non-systemic conventional fungicides were used. These fungicides have been called “multi-site inhibitors” because they non-selectively inhibit several biologically important functions of living fungal cells. The nature of their fungitoxic mechanisms implies that there is little possibility for the development of tolerant mutants because mutation of a single gene cannot overcome the lethal effect of their multisite activity. On the other hand, we have seen emergence of tolerant pathogens with the recently introduced systemic fungicides. Since these systemic fungicides can easily penetrate into plant tissues, they must be selectively toxic to pathogens at concentrations that do not produce phytotoxic effects. Therefore, systemic fungicides have been understood to be “specific-site inhibitors” as they affect biochemically restricted regions of fungal cells. This intrinsic nature of systemic fungicides accelerated the selection of the fungicide-tolerant pathogens that appeared through mutation of a single gene.