Neurospora osmotic sensitive strains with
os-1,
os-2,
os-4 and
os-5 mutations showed cross-resistance to dicarboximides, aromatic hydrocarbons and fludioxonil. 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 (LD
50: 0.087μg/ml) and iprodione (LD
50: 14μg/ml). Another osmotic sensitive mutation
cut did not give resistance to these fungicides. The conidia of wild-type and
cut strains swelled and burst without germination on the medium containing fludioxonil, and bursting of conidia was rescued by high osmotic pressure. Stimulation of glycerol biosynthesis 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 resistant
os-1 mutant strain accumulated substantial quantities of glycerol by 10μg/ml of fludioxonil, but produced less glycerol by 10μg/ml of iprodione. Thus it was assumed that fungal toxicity of these fungicides might be due to abnormal glycerol accumulation. However, both fludioxonil and iprodione did not induce glycerol biosynthesis in the fungicide-sensitive
cut mutant strain. In response to osmotic stress,
os mutant strains accumulated less 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
cut strains were not distinguishable in their modes of fungal toxicity of fludioxonil. These data suggest that dicarboximides, aromatic hydrocarbons and fludioxonil interfere with the osmotic signal transduction pathway resulting in stimulation of glycerol biosynthesis, but abnormal glycerol accumulation is not essential for their fungal toxicity.
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