| Summary: | Endoplasmic reticulum (ER) stress elicits a protective mechanism called unfolded protein response (UPR) to maintain cellular homeostasis, which can be regulated by defence hormones. In this study, the physiological role of jasmonic acid (JA) in ER stress and UPR signalling has been investigated in intact leaves of tomato plants. Exogenous JA treatments not only induced the transcript accumulation of UPR marker gene <i>SlBiP</i> but also elevated transcript levels of <i>SlIRE1</i> and <i>SlbZIP60</i>. By the application of JA signalling mutant <i>jai1</i> plants, the role of JA in ER stress sensing and signalling was further investigated. Treatment with tunicamycin (Tm), the inhibitor of N-glycosylation of secreted glycoproteins, increased the transcript levels of <i>SlBiP</i>. Interestingly, <i>SlIRE1a</i> and <i>SlIRE1b</i> were significantly lower in <i>jai1</i>. In contrast, the transcript accumulation of <i>Bax Inhibitor-1</i> (<i>SlBI1</i>) and <i>SlbZIP60</i> was higher in <i>jai1</i>. To evaluate how a chemical chaperone modulates Tm-induced ER stress, plants were treated with sodium 4-phenylbutyrate, which also decreased the Tm-induced increase in <i>SlBiP</i>, <i>SlIRE1a,</i> and <i>SlBI1</i> transcripts. In addition, it was found that changes in hydrogen peroxide content, proteasomal activity, and lipid peroxidation induced by Tm is regulated by JA, while nitric oxide was not involved in ER stress and UPR signalling in leaves of tomato.
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