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Endoplasmic reticulum-mediated unfolded protein response is an integral part of singlet oxygen signalling in plants.
The Plant Journal ( IF 7.2 ) Pub Date : 2020-01-23 , DOI: 10.1111/tpj.14700
Inès Beaugelin 1 , Anne Chevalier 1 , Stefano D'Alessandro 1 , Brigitte Ksas 1 , Michel Havaux 1
Affiliation  

Singlet oxygen (1O2) is a by‐product of photosynthesis that triggers a signalling pathway leading to stress acclimation or to cell death. By analyzing gene expressions in a 1O2‐overproducing Arabidopsis mutant (ch1 ) under different light regimes, we show here that the 1O2 signalling pathway involves the endoplasmic reticulum (ER)‐mediated unfolded protein response (UPR). ch1 plants in low light exhibited a moderate activation of UPR genes, in particular bZIP60 , and low concentrations of the UPR‐inducer tunicamycin enhanced tolerance to photooxidative stress, together suggesting a role for UPR in plant acclimation to low 1O2 levels. Exposure of ch1 to high light stress ultimately leading to cell death resulted in a marked upregulation of the two UPR branches (bZIP60/IRE1 and bZIP28/bZIP17). Accordingly, mutational suppression of bZIP60 and bZIP28 increased plant phototolerance, and a strong UPR activation by high tunicamycin concentrations promoted high light‐induced cell death. Conversely, light acclimation of ch1 to 1O2 stress put a limitation in the high light‐induced expression of UPR genes, except for the gene encoding the BIP3 chaperone, which was selectively upregulated. BIP3 deletion enhanced Arabidopsis photosensitivity while plants treated with a chemical chaperone exhibited enhanced phototolerance. In conclusion, 1O2 induces the ER‐mediated UPR response that fulfils a dual role in high light stress: a moderate UPR, with selective induction of BIP3 , is part of the acclimatory response to 1O2, and a strong activation of the whole UPR is associated with cell death.

中文翻译:

内质网介导的未折叠蛋白应答是植物中单线态氧信号传导的组成部分。

单线态氧(1 O 2)是光合作用的副产物,它触发信号传导途径,导致压力适应或细胞死亡。通过分析在不同光照条件下1 O 2高产拟南芥突变体(ch1)中的基因表达,我们在这里显示1 O 2信号传导途径涉及内质网(ER)介导的未折叠蛋白应答(UPR)。ch1植物在弱光下表现出中等激活的UPR基因,特别是bZIP60,以及低浓度的UPR诱导剂衣霉素增强了对光氧化胁迫的耐受性,共同表明UPR在植物适应低1 O 2含量中的作用。ch1暴露于高光胁迫下最终导致细胞死亡,导致两个UPR分支(bZIP60 / IRE1和bZIP28 / bZIP17)明显上调。因此,bZIP60bZIP28的突变抑制增加了植物的光耐受性,高衣霉素浓度对UPR的强烈激活促进了高光诱导的细胞死亡。相反,ch11 O 2的光适应压力限制了UPR基因的高光诱导表达,除了编码BIP3伴侣的基因被选择性上调外。BIP3缺失增强了拟南芥的光敏性,而用化学分子伴侣处理的植物则表现出增强的耐光性。总而言之,1 O 2诱导ER介导的UPR反应,在高光胁迫下发挥双重作用:适度的UPR,选择性诱导BIP3,是对1 O 2的适应性反应的一部分,并且强烈激活整个UPR与细胞死亡有关。
更新日期:2020-01-23
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