Endophyte Infection and Methyl Jasmonate Treatment Increased the Resistance of to Insect Herbivores Independently.

Alkaloids are usually thought to be responsible for protecting endophyte-infected (EI) grasses from their herbivores. For EI grasses that produce few alkaloids, can endophyte infection enhance their resistance to herbivores? Related studies are limited. In the Inner Mongolian steppe, is highly infected by endophytes, but produces few alkaloids. Locusts are the common insect herbivores of grasses. In this study, was used as plant material. Methyl jasmonate (MJ, when applied exogenously, can induce responses similar to herbivore damage) treatment was performed. The effects of endophyte infection and MJ treatment on the resistance of to were studied. We found that locusts preferred EF (endophyte-free) plants to EI plants in both choice and no-choice feeding experiments. Endophyte infection enhanced the resistance of to locusts. Endophyte infection decreased soluble sugar concentrations, while it increased the total phenolic content and phenylalanine ammonia lyase (PAL) activity, which may contribute to the resistance of to locusts. There was an interaction effect between MJ treatment and endophyte infection on the growth of the host. MJ treatment was a negative regulator of the plant growth-promoting effects of endophyte infection. There was no interaction effect between MJ treatment and endophyte infection on the defense characteristics of the host. In groups not exposed to locusts, MJ treatment and endophyte infection had a similar effect in decreasing the soluble sugar content, while increasing the total phenolic content and the PAL activity. In groups exposed to locusts, the effect of MJ treatment on the above characteristics disappeared, while the effect of endophyte infection became more obvious. All of these results suggest that even for endophytes producing few alkaloids, they could still increase the resistance of native grasses to insect herbivores. Furthermore, endophyte infection might mediate the defense responses of the host, independent of jasmonic acid (JA) pathways.