Sterol overproduction is the biochemical basis of resistance to a triazole in calli from a tobacco mutant.

Sterol overproduction is shown to be the biochemical basis of resistance to the triazole LAB 170250F (2-(4-chlorophenyl)-3-phenyl-1-(1H-1,2,4-triazol-1-yl)-2,3-oxidopropane), an inhibitor of cytochrome P450-dependent-obtusifoliol-14α-demethylase, in the tobacco ( Nicotiana tabacum L. cv. Xanthi) mutant LAB 1-4. Genetic analysis at the callus level indicates that the resistance and the biochemical phenotypes co-segregate during meiotic recombination and therefore result most probably from the same mutation. Analysis of the intracellular distribution of sterols shows that in LAB 1-4 calli containing tenfold the sterol amount of the wild type, the overproduced metabolites, mainly obtusifoliol, are esterified by fatty acids and stored in hyaloplasmic lipid droplets. Thus, the mutant calli maintain a concentration of free sterols in cell membranes, mainly end-products of the sterol-biosynthesis pathway, which corresponds to physiological requirements, whereas the level of free sterols in the wild-type calli treated with the triazole is too low to ensure viability. We also show that sterol overproduction confers resistance to other phytotoxic sterolbiosynthesis inhibitors. [ABSTRACT FROM AUTHOR]