Endophytic fungus Trichoderma atroviride D16 increases tanshinone accumulation in Salvia miltiorrhiza plantlets by enhancing abscisic acid and salicylic acid signaling

The vast biodiversity of endophytic fungi and its potential to improve the production of bioactive metabolites in host plants has attracted intense research of endophytic fungi. However, extensive research is needed to explore in detail the interaction between specific endophytic fungi, host physiological responses and changes to plant secondary metabolites. The present work shows that an endophytic fungus Trichoderma atroviride D16 can promote the accumulation of tanshinones in the root of S. miltiorrhiza, and also can induce the production of abscisic acid (ABA) and salicylic acid (SA) in the root of S. miltiorrhiza. Pre-treatment of plantlets with biosynthetic inhibitors of ABA or SA blocked the endophytic fungi-induced tanshinones production. ABA inhibitors not only inhibited the accumulation of tanshinones induced by endophytic fungi, but also inhibited the production of ABA and SA; However, SA inhibitors have no obvious inhibition on the biosynthesis of induced ABA, which means that SA plays a role in the downstream of ABA production. These results confirmed that exogenous ABA and SA can reversed the inhibition in the inhibitors on the accumulation of tanshinones induced by endophytic fungi. Endophytic fungi, ABA and SA treatments also significantly increased the transcriptional activity of genes in the tanshinone biosynthesis pathway, the main pathway for endophytic fungi to induce the synthesis of tanshinones was found to be the mevalonate pathway. These results indicate that T. atroviride D16, as an endogenous elicitor, stimulates the biosynthesis of tanshinones in the root of S. miltiorrhiza, thereby yielding additional insight into the interconnection between ABA and SA in biosynthesis-related signaling pathways.