Sensitivity to phenylpyrrole fungicides and abnormal glycerol accumulationin os and cut mutant strains of Neurospora crassa

Neurospora osmotic sensitive strains with os-1, os-2, os-4 and os-5 mutatio ns showed cross-resistance to dicarboximides, aromatic hydrocarbons and flu dioxonil, The os-2, os-4, and os-5 mutant strains were highly resistant to them, while the os-1 mutant strain was moderately resistant and its growth was inhibited by fludioxonil (LD50: 0.087 mu g/ml) and iprodione (LD50: 14 mu g/ml). Another osmotic sensitive mutation cut did not give resistance to these fungicides. The conidia of wild-type and cut strains swelled and bur st without germination on the medium containing fludioxonil, and bursting o f conidia was rescued by high osmotic pressure. Stimulation of glycerol bio synthesis by fludioxonil and iprodione observed in the wild-type strain was not induced in os-2, os-4 and os-5 mutant strains. The moderately resistan t os-1 mutant strain accumulated substantial quantities of glycerol by 10 m u g/ml of fludioxonil, but produced less glycerol by 10 mu g/ml of iprodion e. Thus it was assumed that fungal toxicity of these fungicides might be du e to abnormal glycerol accumulation. However, both fludioxonil and iprodion e did not induce glycerol biosynthesis in the fungicide-sensitive cut mutan t strain. : In response to osmotic stress, os mutant strains accumulated le ss amount of glycerol than the wild-type strain, whereas cut mutant strain did not produce glycerol in the medium containing 4% NaCl. Despite its lack of ability of glycerol biosynthesis in cut mutant strain, wild-type and cu t strains were not distinguishable in their modes of fungal toxicity of flu dioxonil. These data suggest that dicarboximides, aromatic hydrocarbons and fludioxonil interfere with the osmotic signal transduction pathway resulti ng in stimulation of glycerol biosynthesis, but abnormal glycerol accumulat ion is not essential for their fungal toxicity.