| Abstract: | The C-14 demethylation of the sterols, dependent on cytochrome P-450, and the C-22(23) desaturation of sterols are reactions in the ergosterol biosynthesis pathway that are regarded as primary target sites in the toxicity of fungicides of the pyrimidin-5-ylmethanol type. Currently, there is no evidence for target sites in other pathways of comparable sensitivity, although the failure of added ergosterol to reverse the fungitoxicity suggests the existence of such sites. The mitochondrial respiratory systems in Ustilago maydis and Aspergillus nidulans are insensitive to this type of fungicide and are not regarded as primary targets of fungitoxicity in these organisms. Appreciable evidence indicates that the primary targets in higher plant growth regulation are reactions, dependent on cytochrome P-450, that assist in the conversion of kaurene to kaurenoic acid in the gibberellin (GA) biosynthesis pathway. Growth retardation by high concentrations of pyrimidin-5-ylmethanols, which is not reversable by GA, apparently involves action at sites outside the GA biosynthesis pathway. The data derived from various studies of the mechanisms of fungitoxicity and growth regulation suggest that any undetected primary targets of the pyrimidin-5-ylmethanols are likely to be haem enzymes, similar to the cytochrome P-450 involved in sterol C-14 demethylation. |
