This is due to the fact that voriconazole is applied in human and veterinary medicine as an inhibitor of fungal CYP51s, which are sterol 14a-demethylases. CYP51 catalyzes demethylation of lanosterol in mammals and yeasts and demethylation of eburicol in filamentous fungi and is one of the most conserved P450s across the kingdoms. CYP51A2 of arabidopsis converts obtusifoliol by C14-demethylation to 4a-methyl-5a-ergosta-8,14,24 -trien- 3b-ol. A loss of CYP51A2 function results in alterations in sterol levels closely resembling those of voriconazole-treated plants: an accumulation of obtusifoliol and 14a-methyl-D8-sterols at the expense of Dabrafenib campesterol and sitosterol. Moreover, like voriconazole-treated plants, CYP51A2 knock-out mutants showed reduced cell elongation leading to impaired shoot and root development. In addition to these phenotypes, cyp51a2 mutant plants display postembryonic seedling lethality, which is also characteristic for other mutants affected in the conversion of obtusifoliol to 24-methylene-cholesterol and isofucosterol. Seedling lethality phenotypes of fk, hyd1 and smt1 have been attributed to a disturbed embryogenesis and are a maternal Kinase Inhibitor Library effect. Although early embryogenesis is not strongly affected in cyp51a2, the mutant shows impaired seed development. An application of voriconazole to healthy seedlings likely uncoupled the roles of CYP51A2 in the different phases of plant development and thereby revealed specific functions of CYP51A2 products in the seedling stage. Consistent with this hypothesis an application of voriconazole to flowers strongly affected seed development. In this context it is interesting to note that defects in seedling development induced by voriconazole treatment were rescued by BR application. Thus, in the seedling stage the bulk sterols isofucosterol, sitosterol and stigmasterol do not appear to be essential for development and CYP51 is primarily required to supply campesterol, as a precursor for BR production. Our results show that voriconazole acts to inhibit BR-dependent sterol biosynthesis and more specifically, obtusifoliol 14a-demethylase activity in planta. Compounds acting on this activity have been identified previously. However, some of these inhibitors are not specifically targeting sterol production as they additionally inhibit the cytochrome P450-mediated oxidation steps of entkaurene to ent-kaurenoic acid and thereby also reduce GA biosynthesis. As opposed to known GA biosynthesis inhibitors such as paclobutrazol and uniconazole, voriconazole did not reduce the germination efficiency of arabidopsis seeds.