Data from: Response to persistent er stress in plants: a multiphasic process that transitions cells from prosurvival activities to cell death

The unfolded protein response (UPR) is a highly conserved response that protects plants from adverse environmental conditions. The UPR is elicited by endoplasmic reticulum (ER) stress, in which unfolded and misfolded proteins accumulate within the ER. Here, we induced the UPR in maize (Zea mays) seedlings to characterize the molecular events that occur over time during persistent ER stress. We found that a multiphasic program of gene expression was interwoven among other cellular events, including the induction of autophagy. One of the earliest phases involved the degradation by regulated IRE1-dependent RNA degradation (RIDD) of RNA transcripts derived from a family of peroxidase genes. RIDD resulted from the activation of ZmIRE1 for promiscuous ribonuclease activity that attacks the mRNAs of secreted proteins. This was followed by an upsurge in expression of the canonical UPR genes indirectly driven by ZmIRE1 due to its splicing of Zmbzip60 to make an active transcription factor that directly upregulates many of the UPR genes. At the peak of UPR gene expression, a global wave of alternative RNA processing led to the production of many aberrant UPR gene transcripts, likely tempering the ER stress response. During later stages of ER stress, ZmIRE1’s activity declined as did the expression of survival modulating genes, Bax inhibitor1 and Bcl-2-associated athanogene7, amidst a rising tide of cell death. Thus, in response to persistent ER stress, maize seedlings embark on a course of gene expression and cellular events progressing from adaptive responses to cell death.未折叠蛋白反应（unfolded protein response, UPR）是一种高度保守的防御机制，可保护植物免受不良环境胁迫。当内质网（endoplasmic reticulum, ER）中积累未折叠与错误折叠蛋白时，即可诱发UPR。本研究通过诱导玉米（Zea mays）幼苗的未折叠蛋白反应，旨在表征持续性内质网应激过程中随时间进程发生的分子事件。我们发现，多相性基因表达程序与包括细胞自噬（autophagy）诱导在内的其他细胞事件紧密交织。其中最早的阶段之一，是通过调控性IRE1依赖型RNA降解（regulated IRE1-dependent RNA degradation, RIDD）降解一类过氧化物酶基因所产生的RNA转录本。RIDD的发生源于ZmIRE1被激活，获得可靶向攻击分泌蛋白mRNA的泛特异性核糖核酸酶（ribonuclease）活性。在此之后，经典未折叠蛋白反应基因的表达出现显著上调，该过程由ZmIRE1间接介导：ZmIRE1通过剪接Zmbzip60，生成具有活性的转录因子，后者可直接上调多数未折叠蛋白反应基因的表达。在未折叠蛋白反应基因表达达到峰值时，全局范围的可变RNA加工（alternative RNA processing）浪潮催生了大量异常的未折叠蛋白反应基因转录本，这可能会减弱内质网应激反应。在内质网应激的后期阶段，ZmIRE1的活性下降，存活调节基因Bax抑制剂1（Bax inhibitor1）与Bcl-2相关蛋白7（Bcl-2-associated athanogene7）的表达水平也随之降低，与此同时细胞死亡的浪潮不断攀升。综上，当面临持续性内质网应激时，玉米幼苗会启动一系列基因表达与细胞事件程序，其进程从适应性响应逐步转向细胞死亡。