前言 | 环境和生理状况会影响内质网蛋白质合成与折叠能力之间的平衡,并导致内质网应激, 这是一种潜在的致命状况。当内质网应激无法解决时,未折叠蛋白反应(UPR) 会恢复内质网稳态或启动程序性细胞死亡(PCD)。 细胞命运决定机制尚不清楚,尤其是在植物中。 |
在这项研究中,作者整合了遗传学和内质网应激谱分析,结合模式物种拟南芥350个自然来源的材料的自然变异和数量性状位点分析。
Pastor-Cantizano et al 的分析将导致一般性细胞死亡调节因子 BON-ASSOCIATED PROTEIN2 (BAP2) 功能丧失的单核苷酸多态性 与 UPR 结果联系起来。
Pastor-Cantizano et al 确立了内质网应激诱导的 BAP2 表达受到内质网应激主要调节因子 inositol-requiring enzyme 1 (IRE1) 的拮抗调控,并且 BAP2 在内质网应激中控制适应性 UPR 幅度并在 UPR 不足的情况下启动促死亡机制。
During the adaptive phase of the UPR, IRE1 activates pro-survival strategies to outweigh constitutive pro-death processes. In this model, BAP2 functions as a rheostat that monitors IRE1 function to prevent irreversible outcomes, while IRE1 controls BAP2 levels as a negative feedback loop for an optimization of UPR sufficiency. During this phase, IRE1 and BAP2 may induce NAC089 expression as a preventive process for NAC089 requirement to ignite PCD when the UPR becomes insufficient in unresolved ER stress. When the latter takes place, BAP2 acts as a pro-death effector, leading to H2O2 accumulation and PCD as an irreversible step that outweighs pro-life adaptations. Therefore, cell-fate determination under ER stress is the result of a tug-of-war between pro-life and pro-death processes. Continuous arrows indicate direct known effects and dotted arrows indicate indirect effects. Created with BioRender.com.
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原创深度解析:移动mRNA,双链RNA受体,蛋白翻译参与的植物免疫,TOR信号与再生,CaMV,TOR与光信号,TOR与RNA可变剪切,
客户文章精选:TOR-4EBP,荔枝脱落,CUCUME数据库,伴侣蛋白辅助RNP运输,二价染色质与环境响应。
原创锐评:Science子刊错误的数据分析,Nature糟糕的审稿,Elsevier的贪婪,经常被忽略的植物学研究,顶刊忽视预印,拉大牛入伙,科研评价体系,一稿多投,让人失望的Plant Journal,Current Biology发文良莠不齐。
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