N-[5-(Trifluoromethyl)pyridin-2-yl]benzenesulfonamide partially mimics methyl jasmonate without growth inhibition in Nicotiana benthamiana

Abstract

Jasmonates (JAs) are phytohormones that induce plant defense responses against pathogens and herbivores. However, JAs often cause plant growth inhibition. Thus, JAs have not been practically useful for crop protection to date. In this study, we demonstrate that N-[5-(Trifluoromethyl)pyridin-2-yl]benzenesulfonamide (TPBS) can upregulate JA-inducible defense genes in Nicotiana benthamiana plants without severe growth inhibition. Using a promoter-luciferase-based high-throughput system (HTS) in Arabidopsis thaliana seedlings, TPBS was found to be an agonist of methyl jasmonate (MeJA)-dependent responses, although TPBS has no structural similarity to MeJA. MeJA strongly upregulates the expression of many secondary metabolite-related genes involved in five major secondary metabolic pathways: the alkaloid, terpenoid, phenylpropanoid, flavonoid, and anthocyanin pathways. TPBS application significantly upregulated only some of these genes in the roots, mainly those involved in the alkaloid biosynthesis pathways. The biological activity of TPBS was tested according to its ability to increase the accumulation of nicotine, a well-known JA-inducible alkaloid involved in defense responses. TPBS led to accumulation of nicotine as much as MeJA in N. benthamiana leaves. We found that 10 μM TPBS led to nicotine accumulation (9.7-fold) without growth inhibition (104%), indicating that TPBS can uncouple defense responses from growth inhibition. These features make TPBS a strong candidate for use in crop protection, as demonstrated by increased nicotine content in tobacco.

Keywords

• Nicotiana benthamiana Solanaceae
• Methyl jasmonate
• Agonist
• Alkaloids
• Nicotine