| Summary: | Jasmonates (JAs), the group of lipid-derived hormones, were found to control the defense responses in a myriad of plants. Meaningfully, the macrolactones of 12-hydroxy jasmonate isoleucine (12OH-JA-Ile) were reported to induce the defensive response of wild tobacco. However, little to nothing has been known about the elicitation effect of JA-Ile-macrolactones on woody plants to harmful organisms, let alone its underlying mechanisms. Here, we first optimized the synthetic routine using mild toxic reagent isobutyl chloroformate instead of ethyl chloroformate for conjugation, and we used acetonitrile (MeCN) instead of ethyl alcohol for the better dissolution of <i>p</i>-toluenesulfonic acid (<i>p</i>-TsOH) to gain JA-Ile-macrolactones. JA-Ile-macrolactone <b>5b</b>-treated tea plants significantly inhibited the larvae weight gain of <i>Ectropis obliqua</i> larvae and the lesions caused by <i>Colletotrichum camelliae</i>. Furthermore, the expression level of <i>CsOPR3</i> was significantly upregulated in <b>5b</b>-treated leaves. Meanwhile, <b>5b</b> reduced the accumulation of eriodictyol 7-O-glucuronide (EDG) in tea plants, which was confirmed to promote the growth rate of <i>E. obliqua</i> larvae by artificial diet assay. In conclusion, our study proved that the exogenous application of <b>5b</b> could induce the tea plant resistance both to herbivore <i>E. obliqua</i> and pathogen <i>C. camelliae</i>, and EDG was identified as one of the secondary metabolites that could influence the growth rate of <i>E. obliqua</i>, but it did not directly influence the infection of <i>C. camelliae</i> in vitro. Further research should be carried out to clarify the mechanism through which <b>5b</b> induces tea plant resistance to <i>C. camelliae</i>.
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