各种胁迫因子引起内质网(Endoplasmic Reticulum, ER)蛋白折叠失衡，引发ER胁迫。动物三种ER受体ATF6、IRE1及PERK感应ER胁迫，激活下游防御机制。拟南芥中仅发现有类似ATF6及IRE1途径，类似PERK的蛋白翻译调控在植物界尚未报道。申请人之前筛选到拟南芥突变体lew1，由于蛋白糖基化受损而产生较多错误折叠的蛋白，更早地激活了ER信号防御机制，比野生型更抗干旱。EMS诱变lew1，申请人筛选到抗旱表型恢复的突变体sol1，已找到突变位点，初步表明SOL1在类似PERK介导的蛋白翻译调控中起作用。本项目以突变体lew1、lew1sol1及sol1为材料，通过生理生化、转录组分析及蛋白技术等，阐明SOL1在ER蛋白翻译调控中的作用机理，揭示ER蛋白翻译调控在植物抗旱中的作用，为植物抗旱研究及ER信号途径开辟新路径，同时为改良作物的抗旱性及抗旱育种提供理论基础。

Intracellular perturbations such as cellular Ca2+ concentration or redox homeostasis caused by a variety of stressors, e.g. viral infection, energy deprivation, NH4+ toxicity, heat stress, drought or salt stress, induce the unbalance of protein folding, leading to the accumulation of unfolded proteins and endoplasmic reticulum (ER) stress. In mammalian cells, there are three ER receptors including activating transcription factor 6 (ATF6), inositol requiring kinase 1 (IRE1) and double-stranded RNA-activated protein kinase (PKR)-like endoplasmic reticulum kinase (PERK), which sense ER stress signals and activate the downstream response trying to reestablish the balance of protein folding. In Arabidopsis, bZIP17 and bZIP28, similar to ATF6, and bZIP60 as the target of IRE1, were reported in ER stress signals. However, the PERK pathway sensing ER stress to regulate protein translation was neither reported in plants. An Arabidopsis mutant lew1 (leaf wilting 1), isolated by the applicant, activates earlier ER signals to reestablish the balance of protein folding than wild type, due to unfolded proteins caused by a certain defect of protein glycosylation, so that mutants lew1 are more resistant to drought stress than wild type. The applicant mutagenized the drought-resistant mutants lew1 and isolated a recovered mutant sol1 (suppressor of lew1 1). The mutation site of sol1 has been found, and primary evidences show that SOL1 mediates protein translation in ER stress signaling, suggesting that plants slow down protein translation to reduce the demand of protein folding in drought stress conditions, similar to PERK pathway in animals.The application aims to uncover the mechanism of SOL1 in controlling protein translation and the adaptive regulation of protein translation in drought stress, using mutants lew1, lew1sol1 and sol1 as the materials. By means of physilogical analysis, biochemical assays, profile analysis of gene expression and protein technology, the adaptive mechanism of SOL1 in ER signaling to regulate protein translation in response to drought stress will be disclosed, as a new pathway of drought stress and ER stress signaling in plants and the rationale to increase the resistant ability to drought stress in crops by genetic engineering and traditional breeding.