Summary Plants produce and emit terpenes, including sesquiterpenes, during growth and development, which serve different functions in plants. The sesquiterpene nerolidol has health‐promoting properties and adds a floral scent to plants. However, the glycosylation mechanism of nerolidol and its biological roles in plants remained unknown. Sesquiterpene UDP‐glucosyltransferases were selected by using metabolites‐genes correlation analysis, and its roles in response to cold stress were studied. We discovered the first plant UGT (UGT91Q2) in tea plant, whose expression is strongly induced by cold stress and which specifically catalyzes the glucosylation of nerolidol. The accumulation of nerolidol glucoside was consistent with the expression level of UGT91Q2 in response to cold stress, as well as in different tea cultivars. The reactive oxygen species (ROS) scavenging capacity of nerolidol glucoside was significantly higher than that of free nerolidol. Down‐regulation of UGT91Q2 resulted in reduced accumulation of nerolidol glucoside, ROS scavenging capacity and tea plant cold tolerance. Tea plants absorbed airborne nerolidol and converted it to its glucoside, subsequently enhancing tea plant cold stress tolerance. Nerolidol plays a role in response to cold stress as well as in triggering plant–plant communication in response to cold stress. Our findings reveal previously unidentified roles of volatiles in response to abiotic stress in plants.
Plants emit a variety of volatiles in response to herbivore attack, and (Z)‐3‐hexenol and its glycosides have been shown to function as defence compounds. Although the ability to incorporate and convert (Z)‐3‐hexenol to glycosides is widely conserved in plants, the enzymes responsible for the glycosylation of (Z)‐3‐hexenol remained unknown until today. In this study, uridine‐diphosphate‐dependent glycosyltransferase (UGT) candidate genes were selected by correlation analysis and their response to airborne (Z)‐3‐hexenol, which has been shown to be taken up by the tea plant. The allelic proteins UGT85A53‐1 and UGT85A53‐2 showed the highest activity towards (Z)‐3‐hexenol and are distinct from UGT85A53‐3, which displayed a similar catalytic efficiency for (Z)‐3‐hexenol and nerol. A single amino acid exchange E59D enhanced the activity towards (Z)‐3‐hexenol, whereas a L445M mutation reduced the catalytic activity towards all substrates tested. Transient overexpression of CsUGT85A53‐1 in tobacco significantly increased the level of (Z)‐3‐hexenyl glucoside. The functional characterization of CsUGT85A53 as a (Z)‐3‐hexenol UGT not only provides the foundation for the biotechnological production of (Z)‐3‐hexenyl glucoside but also delivers insights for the development of novel insect pest control strategies in tea plant and might be generally applicable to other plants.
Interleukin-8 (IL-8) is a common inflammatory factor, which involves in various non-specific pathological processes of inflammation. It has been found that increased endothelial permeability accompanied with high expression of IL-8 at site of injured endothelium and atherosclerotic plaque at early stages, suggesting that IL-8 participated in regulating endothelial permeability in the developing processes of vascular disease. The purpose of this study is to investigate the regulation effects of IL-8 on the vascular endothelial permeability, and the mRNA and protein expression of tight junction components (i.e., ZO-1, Claudin-5 and Occludin). Endothelial cells were stimulated by IL-8 with the dose of 50, 100 and 200 ng/mL, and duration of 2, 4, 6, 8h, respectively. The mRNA and protein expression level of tight junction components with IL-8 under different concentration and duration was examined by RT-PCR and Western blot, respectively. Meanwhile, the integrins induced focal adhesions event with IL-8 stimulation was also investigated. The results showed that IL-8 regulated the permeability of endothelium by down-regulation of tight junction in a dose- and time-dependence manner, but was not by integrins induced focal adhesions. This finding reveals the molecular mechanism in the increase of endothelial cell permeability induced by IL-8, which is expected to provide a new idea as a therapeutic target in vascular diseases.
Herbivore‐induced plant volatiles play important ecological roles in defense against stresses. However, if and which volatile(s) are involved in the plant–plant communication in response to herbivorous insects in tea plants remains unknown. Here, plant–plant communication experiments confirm that volatiles emitted from insects‐attacked tea plants can trigger plant resistance and reduce the risk of herbivore damage by inducing jasmonic acid (JA) accumulation in neighboring plants. The emission of six compounds was significantly induced by geometrid Ectropis obliqua, one of the most common pests of the tea plant in China. Among them, (E)‐4,8‐dimethyl‐1,3,7‐nonatriene (DMNT) could induce the accumulation of JA and thus promotes the resistance of neighboring intact plants to herbivorous insects. CsCYP82D47 was identified for the first time as a P450 enzyme, which catalyzes the final step in the biosynthesis of DMNT from (E)‐nerolidol. Down‐regulation of CsCYP82D47 in tea plants resulted in a reduced accumulation of DMNT and significantly reduced the release of DMNT in response to the feeding of herbivorous insects. The first evidence for plant–plant communication in response to herbivores in tea plants will help to understand how plants respond to volatile cues in response to herbivores and provide new insight into the role(s) of DMNT in tea plants.
The endomembrane system is an interconnected network required to establish signal transduction, cell polarity, and cell shape in response to developmental or environmental stimuli. In the model plant , there are numerous markers to visualize polarly localized plasma membrane proteins utilizing endomembrane trafficking. Previous studies have shown that the large ARF-GEF GNOM plays a key role in the establishment of basal (rootward) polarity, whereas the apically (shootward) polarized membrane proteins undergo sorting via different routes. However, the mechanism that maintains apical polarity is largely unknown. Here, we used a chemical genomic approach and identified the compound endosidin 16 (ES16), which perturbed apically localized plasma membrane proteins without affecting basal polarity. We demonstrated that ES16 is an inhibitor for recycling of apical, lateral, and nonpolar plasma membrane proteins as well as biosynthetic secretion, leaving the basal proteins as the only exceptions not subject to ES16 inhibition. Further evidence from pharmaceutical and genetic data revealed that ES16 effects are mediated through the regulation of small GTPase RabA proteins and that RabA GTPases work in concert with the BIG clade ARF-GEF to modulate the nonbasal trafficking. Our results reveal that ES16 defines a distinct pathway for endomembrane sorting routes and is essential for the establishment of cell polarity.
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