Abstract
This paper showed that GSNOR mediated betulin production from genetic and pharmacological levels. The aim of this study was to investigate the relationship between S-nitrosoglutathione reductase (GSNOR) and betulin production. Treatment of birch suspension cells with 20 μmol/L GSNOR inhibitor 3-(5-(4-(1H-imidazol-1-yl) phenyl)-1-(4-carbamoyl-2-methylphenyl)-1H-pyrrol-2-yl) propio- nic acid (N6022) markedly reduced gene expression of GSNOR, and increased at least two times in betulin content and gene expression of lupeol synthase (LUS), a key enzyme in betulin biosynthesis. GSNOR transgenic plants by RNAi silencing also lowered gene expression of GSNOR and increased betulin content and gene expression of LUS. Our study also showed that S-nitrosothiols (SNO) content increased in birch suspension cells treated with N6022 and GSNOR transgenic birch plants, about three times that in the non-transgenic birch. The above results verified that GSNOR deficiency mediated betulin production from genetic and pharmacological levels, and indicated that protein S-nitrosylation mediated plant secondary metabolite production.
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