过量表达内质网小分子热激蛋白增强番茄的衣霉素抗性

真核细胞内质网腔内未折叠蛋白的过度积累会引起内质网胁迫（ER胁迫），继而激活未折叠蛋白应答（UPR）信号途径，诱导内质网定位的分子伴侣的大量表达（如BiP和calnexin等）。本工作将CaMV35S启动子驱动的内质网小分子热激蛋白基因（ER-sHSP）导入番茄，发现ER-sHSP的过量表达提高了转基因番茄整株对衣霉素的抗性。衣霉素处理使未转基因番茄中BiP和calnexin基因的表达迅速升高，转基因番茄中这两个基因的表达也有增加，但表达强度明显低于未转基因番茄。说明ER-sHSP能够减轻ER胁迫，并可能参与UPR信号转导途径。

Overexpression of Small Heat-Shock Protein of Endoplasmic Reticulum Enhances Resistance of Tomato to Tunicamycin

The accumulation of unfolded proteins in the endoplasmic reticulum (ER) lumen causes ER stress response in eukaryote cells, activates the unfolded protein response (UPR) and consequently induces the expression of ER-located molecular chaperones (such as BiP, calnexin, etc.). In this study, the full-length small heat-shock protein of endoplasmic reticulum cDNA (ER-sHSP) under the control of CaMV 35S promoter was introduced into tomato by Agrobacterium tumefactions mediated method (Fig.1, Table 1). Overexpression of ER- sHSP enhanced the resistance of the transgenic plant to tunicamycin (Fig.2, Table 2), an inducer of ER stress. Tunicamycin treatment induced anincrease in mRNA level of BiP and calnexin in plant cell, but mRNAs of these two genes in transgenic plants were accumulated to a much smaller extent than those in non-transgenic plants (Fig.3). These results indicated that ER-sHSP could alleviate the ER stress and may be involved in the UPR signal transmission pathway.