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镉处理诱导拟南芥内质网应激和未折叠蛋白反应。

Cadmium treatment induces endoplasmic reticulum stress and unfolded protein response in Arabidopsisthaliana.

作者信息

De Benedictis Maria, Gallo Antonia, Migoni Danilo, Papadia Paride, Roversi Pietro, Santino Angelo

机构信息

Institute of Sciences of Food Production, C.N.R., Unit of Lecce, Lecce, Italy.

Laboratory of General and Inorganic Chemistry, Di.S.Te.B.A. (Dipartimento di Scienze e Technologie Biologic e Ambientali), University of Salento, Lecce, Italy.

出版信息

Plant Physiol Biochem. 2023 Mar;196:281-290. doi: 10.1016/j.plaphy.2023.01.056. Epub 2023 Jan 31.

DOI:10.1016/j.plaphy.2023.01.056
PMID:36736010
Abstract

We report about the response of Arabidopsis thaliana to chronic and temporary Cd stress, and the Cd induced activation of ER stress and unfolded protein response (UPR). Cd-induced UPR proceeds mainly through the bZIP60 arm, which in turn activates relevant ER stress marker genes such as BiP3, CNX, PDI5 and ERdj3B in a concentration- (chronic stress) or time- (temporary stress) dependent manner. A more severe Cd-stress triggers programmed cell death (PCD) through the activation of the NAC089 transcription factor. Toxic effects of Cd exposure are reduced in the Atbzip28/bzip60 double mutant in terms of primary root length and fresh shoot weight, likely due to reduced UPR and PCD activation. We also hypothesised that the enhanced Cd tolerance of the Atbzip28/bzip60 double mutant is due to an increase in brassinosteroids signaling, since the amount of the brassinosteroid insensitive1 receptor (BRI1) protein decreases under Cd stress only in Wt plants. These data highlight the complexity of the UPR pathway, since the ER stress response is strictly related to the type of the treatment applied and the multifaceted connections of ER signaling. The reduced sensing of Cd stress in plants with UPR defects can be used as a novel strategy for phytoremediation.

摘要

我们报道了拟南芥对慢性和暂时镉胁迫的响应,以及镉诱导的内质网应激和未折叠蛋白反应(UPR)的激活。镉诱导的UPR主要通过bZIP60途径进行,进而以浓度(慢性胁迫)或时间(暂时胁迫)依赖的方式激活相关内质网应激标记基因,如BiP3、CNX、PDI5和ERdj3B。更严重的镉胁迫通过激活NAC089转录因子触发程序性细胞死亡(PCD)。在Atbzip28/bzip60双突变体中,镉暴露的毒性作用在初生根长度和地上部鲜重方面有所降低,这可能是由于UPR和PCD激活减少所致。我们还推测,Atbzip28/bzip60双突变体对镉耐受性增强是由于油菜素类固醇信号传导增加,因为仅在野生型植物中,镉胁迫下油菜素类固醇不敏感1受体(BRI1)蛋白的量会减少。这些数据突出了UPR途径的复杂性,因为内质网应激反应与所应用的处理类型以及内质网信号传导的多方面联系密切相关。在具有UPR缺陷的植物中对镉胁迫的感知降低可作为植物修复的一种新策略。

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Cadmium treatment induces endoplasmic reticulum stress and unfolded protein response in Arabidopsisthaliana.镉处理诱导拟南芥内质网应激和未折叠蛋白反应。
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