(+)-Catechin, epicatechin and epigallocatechin gallate are important inducible defensive compounds against Ectropis grisescens in tea plants.

The tea plant, Camellia sinensis (L.) O. Kuntze, is an economically important, perennial woody plant rich in catechins. Although catechins have been reported to play an important role in plant defences against microbes, their roles in the defence of tea plants against herbivores remain unknown. In this study, we allowed the larvae of Ectropis grisescens, a leaf-feeding pest, to feed on the plants, and alternatively, we wounded the plants and then treated them with E. grisescens oral secretions (WOS). Both approaches triggered jasmonic acid-, ethylene- and auxin-mediated signalling pathways; as a result, plants accumulated three catechin compounds: (+)-catechin, epicatechin and epigallocatechin. Not only was the mass of E. grisescens larvae fed on plants previously infested with E. grisescens or treated with WOS significantly lower than that of larvae fed on controls, but also artificial diet supplemented with epicatechin, (+)-catechin or epigallocatechin gallate reduced larval growth rates. In addition, the exogenous application of jasmonic acid, ethylene or auxin induced the biosynthesis of the three catechins, which, in turn, enhanced the resistance of tea plants to E. grisescens, leading to the coordination of the three signalling pathways. Our results suggest that the three catechins play an important role in the defences of tea plants against E. grisescens.

Genome-Wide Identification of the Tify Gene Family and Their Expression Profiles in Response to Biotic and Abiotic Stresses in Tea Plants (Camellia sinensis).

The TIFY family is a plant-specific gene family that is involved in regulating a variety of plant processes, including developmental and defense responses. The chromosome-level genome of the tea plant (Camellia sinensis) has recently been released, but a comprehensive view of the TIFY family in C. sinensis (the CsTIFY genes) is lacking. The current study performed an extensive genome-wide identification of CsTIFY genes. The phylogenetics, chromosome location, exon/intron structure, and conserved domains of these genes were analyzed to characterize the members of the CsTIFY family. The expression profiles of the CsTIFY genes in four organs were analyzed, and they showed different spatial expression patterns. All CsJAZ genes were observed to be induced by jasmonate acid (JA) and exhibited different responses to abiotic and biotic stresses. Six of seven CsJAZ genes (CsJAZ1, CsJAZ2, CsJAZ3, CsJAZ4, CsJAZ7, and CsJAZ8) were upregulated by mechanical wounding and infestation with the tea geometrid (Ectropis obliqua), while infection with tea anthracnose (Colletotrichum camelliae) primarily upregulated the expression levels of CsJAZ1 and CsJAZ10. In addition, CsJAZs were observed to interact with CsMYC2 and AtMYC2. Therefore, the results of this study may contribute to the functional characterization of the CsTIFY genes, especially the members of the JAZ subfamily, as regulators of the JA-mediated defense response in tea plant.

JA-Ile-macrolactone 5b Induces Tea Plant (Camellia sinensis) Resistance to Both Herbivore Ectropis obliqua and Pathogen Colletotrichum camelliae.

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 p-toluenesulfonic acid (p-TsOH) to gain JA-Ile-macrolactones. JA-Ile-macrolactone 5b-treated tea plants significantly inhibited the larvae weight gain of Ectropis obliqua larvae and the lesions caused by Colletotrichum camelliae. Furthermore, the expression level of CsOPR3 was significantly upregulated in 5b-treated leaves. Meanwhile, 5b reduced the accumulation of eriodictyol 7-O-glucuronide (EDG) in tea plants, which was confirmed to promote the growth rate of E. obliqua larvae by artificial diet assay. In conclusion, our study proved that the exogenous application of 5b could induce the tea plant resistance both to herbivore E. obliqua and pathogen C. camelliae, and EDG was identified as one of the secondary metabolites that could influence the growth rate of E. obliqua, but it did not directly influence the infection of C. camelliae in vitro. Further research should be carried out to clarify the mechanism through which 5b induces tea plant resistance to C. camelliae.

The Jasmonic Acid Pathway Positively Regulates the Polyphenol Oxidase-Based Defense against Tea Geometrid Caterpillars in the Tea Plant (Camellia sinensis).

Polyphenol oxidases (PPOs) as inducible defense proteins, contribute to tea (Camellia sinensis) resistance against tea geometrid larvae (Ectropis grisescens), and this resistance has been associated with the jasmonic acid (JA) signaling by testing geometrid performance in our previous work. However, the regulation of PPO-based defense by JA and other hormone signaling underlying these defense responses is poorly understood. Here, we investigated the role of phytohormones in regulating the PPO response to tea geometrids. We profiled levels of defense hormones, PPO activity and CsPPO genes in leaves infested with tea geometrids. Then, hormone levels were manipulated by exogenous application of methyl jasmonate (MeJA), gibberellin acid (GA3), abscisic acid (ABA), JA biosynthesis inhibitors (sodium diethyldithiocarbamate trihydrate, DIECA and salicylhydroxamic acid, SHAM) and GA inhibitor (uniconazole, UNI). Upon geometrid attack, JA levels significantly increased, whereas GA levels notably decreased and ABA level was slightly decreased. And the PPO activity significantly increased in line with the transcript levels of CsPPO2 and CsPPO4 but not CsPPO1. There were an obvious antagonistic cross-talk between JA and GA signals and an association among JA signals, PPO response and herbivore resistance in tea plants. Pretreatment with MeJA increased PPO activity by activating the transcripts of CsPPO2 and CsPPO4, whereas application of JA inhibitor DIECA suppressed PPO activity. GA3 strongly enhanced PPO activity, but ABA did not alter PPO activity. These findings strongly suggest that JA is a central player in PPO-mediated tea resistance against tea geometrids in a manner that prioritizes defense over growth.