Plant potexvirus and potyvirus infection can trigger endoplasmic reticulum (ER) stress. ER stress signaling increases the expression of cytoprotective ER-chaperones, especially the BiP chaperones which contribute to pro-survival functions when plants are subjected to infection. The inositol requiring enzyme (IRE1) is one ER stress sensor that is activated to splice the bZIP60 mRNA which produces a truncated transcription factor that activates gene expression in the nucleus. The IRE1/bZIP60 pathway is associated with restricting potyvirus and potexvirus infection. Recent data also identified the IRE1-independent UPR pathways led by bZIP28 and bZIP17 contribute to potexvirus and potyvirus infection. These three bZIP pathways recognize cis-regulatory elements in the BiP promoters to enhance gene expression. BiP is part of a negative feedback loop that regulates the activities of the ER stress transducers IRE1, bZIP28, and bZIP17 to block their activation. We discuss a model in which bZIP60 and bZIP17 synergistically induce BiP and other genes restricting Plantago asiatica mosaic virus (PlAMV; a potexvirus) infection while bZIP60 and bZIP28 independently induce genes supporting PlAMV infection. Regarding Turnip mosiac virus (TuMV, a potyvirus) infection, bZIP60 and bZIP28 serve to repress local and systemic infection. Finally, tauroursodeoxycholic acid treatments were used to demonstrate that the protein folding capacity significantly influences PlAMV accumulation.

植物potexvirus和potyvirus感染可以触发内质网（ER）压力。内质网应激信号增加了细胞保护性内质伴侣的表达，特别是当植物受到感染时有助于生存功能的BiP分子伴侣。肌醇需求酶（IRE1）是一种ER应激传感器，被激活以剪接bZIP60 mRNA，产生可激活细胞核中基因表达的截短转录因子。IRE1 / bZIP60途径与限制马铃薯痘病毒和马铃薯痘病毒的感染有关。最近的数据还确定了由bZIP28和bZIP17引导的非IRE1的UPR通路与potexvirus和potyvirus感染有关。这三个bZIP途径识别顺式BiP启动子中的调控元件，以增强基因表达。BiP是负反馈回路的一部分，该负反馈回路调节ER应力传感器IRE1，bZIP28和bZIP17的活动以阻止其激活。我们讨论了一个模型，其中bZIP60和bZIP17协同诱导BiP和其他基因限制车前草花叶病毒（PlAMV； potexvirus）感染，而bZIP60和bZIP28独立诱导支持PlAMV感染的基因。关于芜菁莫西亚病毒（TuMV，一种杯状病毒）感染，bZIP60和bZIP28可以抑制局部和全身感染。最后，牛磺去氧胆酸处理用于证明蛋白质折叠能力显着影响P1AMV的积累。