Abstract

Although smoke-isolated butenolide (KAR1) has shown stimulatory effects on secondary metabolite production in medicinal plants, the influence of KAR1 on the accumulation of secondary metabolites in endophytes isolated from medicinal plants has not been reported. This study was initiated to investigate the effects of KAR1 on tanshinone I (T-I) production in the endophyte Trichoderma atroviride D16 isolated from Salvia miltiorrhiza and the involved underlying signal transduction. The results showed that KAR1-induced jasmonic acid (JA), followed by an enhancement in T-I production in T. atroviride D16. External treatment of jasmonic acid methyl ester (JAMe) stimulated the accumulation of T-I without KAR1 treatment. KAR1-induced T-I was suppressed by JA synthesis inhibitors salicylhydroxamic acid (SHAM) and n-propylgallate (PrGall), which indicated that JA played an essential part in KAR1-induced production of T-I. In addition, SHAM and PrGall could not completely inhibit KAR1-inducedT-I, indicating that other signal molecule could be involved in KAR1-induced increase of T-I in case JA pathway was blocked. This study indicated that JA served as a signal role in KAR1-induced T-I production in T. atroviride D16.

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