Exogenous methyl jasmonate prevents necrosis caused by mechanical wounding and increases terpenoid biosynthesis in Panax ginseng

Abstract

Upon mechanical wounding, plants locally induce necrosis, accumulate methyl jasmonate (MeJA) and acquire systemic resistance in nearby tissues. One-month-old in vitro grown Panax ginseng seedlings were treated with either 50 µM MeJA or mechanical wounding alone or a combination of both, to evaluate jasmonic acid (JA) signaling and terpene biosynthetic pathway genes along with terpenoid accumulation. After MeJA treatment, JA pathway genes, such as lipoxygenase (PgLOX), hydrogen peroxidase lyase (PgHPL), allene oxide synthase (PgAOS), and allene oxide cyclase (PgAOC1), and terpene pathway genes, such as isopentenyl diphosphate isomerase (PgIPP) and farnesyl diphosphate synthase (PgFPS), were highly expressed and resulted in the accumulation of mono- and sesquiterpenes. During mechanical wounding, PgLOX expression was induced relatively late after 72 h of treatment, however PgAOC1 was not induced. This resulted in decreased production of MeJA that in turn may have lowered terpenoid production. In contrast, wounding + MeJA treatment increased PgAOC1 and PgLOX gene expression earlier after 6 h and slowly promoted the production of mono- and sesquiterpenes. Furthermore, we monitored the effect of MeJA upon wounding in in vitro grown 1-month-old seedlings treated with MeJA + wounding. These result demonstrated that exogenous MeJA is able to promote recovery from the wounding effect by functioning as a long distance signal. Additionally, these results suggest that exogenous MeJA supplied at the time of mechanical wounding prevents necrosis in the ginseng leaves by increasing the production of terpenoids.