Respiratory burst oxidase homologue-dependent H2.O2. and chloroplast H2.O2. are essential for the maintenance of acquired thermotolerance during recovery after acclimation

Respiratory burst oxidase homologue-dependent H2.O2. and chloroplast H2.O2. are essential for the maintenance of acquired thermotolerance during recovery after acclimation
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呼吸爆发氧化酶同系物依赖性 H2.O2。

DOI:
10.1111/pce.13351
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发表时间:
2018
期刊:
Plant, Cell and Environment
影响因子:
--
通讯作者:
Zhen Wu
Zhen Wu
中科院分区:
其他
文献类型:
--
作者:
Mintao Sun;Fangling Jiang;Benjian Cen;Junqin Wen;Yanzhao Zhou;Zhen Wu

文献摘要

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耐热性是通过热胁迫(HS)驯化而提高的,耐热性水平被植物“记住”。然而,潜在的信号机制在很大程度上仍不清楚。在此,我们发现,在HS驯化后的恢复过程中,NADPH氧化酶介导的H_2O_2(NADPH-H_2O_2)和叶绿体-H_2O_2分别促进HS反应基因和程序性细胞死亡(PCD)基因的持续表达。在HS驯化后喷施NADPH氧化酶抑制剂二苯基碘时,NADPH-H_2O_2水平显著降低,导致HS反应基因表达减少,丧失获得性耐热性(MAT)。相反,与HS驯化相比,HS过度驯化后的恢复过程中,NADPH-H_2O_2下降,而叶绿体-H_2O_2进一步增强,导致HS反应基因表达减少,PCD大量产生。值得注意的是,HS过度驯化后NADPH-H_2O_2的进一步抑制也抑制了叶绿体-H_2O_2,缓解了严重的PCD,超过了HS过度驯化处理。由于HS驯化后亚细胞H_2O_2的变化,番茄幼苗在恢复过程中保持恒定的H_2O_2水平,导致在恢复后进行的HS测试中总H_2O_2水平稳定且较低。我们的结论是,番茄幼苗在恢复过程中通过增加NADPH-H_2O_2含量和控制叶绿体-H_2O_2的产生来增加其MAT,从而分别增强HS反应基因的表达和平衡PCD水平。
Thermotolerance is improved by heat stress (HS) acclimation, and the thermotolerance level is “remembered” by plants. However, the underlying signalling mechanisms remain largely unknown. Here, we showed NADPH oxidase‐mediated H2O2(NADPH‐H2O2), and chloroplast‐H2O2promoted the sustained expression of HS‐responsive genes and programmed cell death (PCD) genes, respectively, during recovery after HS acclimation. When spraying the NADPH oxidase inhibitor, diphenylene iodonium, after HS acclimation, the NADPH‐H2O2level significantly decreased, resulting in a decrease in the expression of HS‐responsive genes and the loss of maintenance of acquired thermotolerance (MAT). In contrast, compared with HS acclimation, NADPH‐H2O2declined but chloroplast‐H2O2further enhanced during recovery after HS over‐acclimation, resulting in the reduced expression of HS‐responsive genes and substantial production of PCD. Notably, the further inhibition of NADPH‐H2O2after HS over‐acclimation also inhibited chloroplast‐H2O2, alleviating the severe PCD and surpassing the MAT of HS over‐acclimation treatment. Due to the change in subcellular H2O2after HS acclimation, the tomato seedlings maintained a constant H2O2level during recovery, resulting in stable and lower total H2O2levels during a tester HS challenge conducted after recovery. We conclude that tomato seedlings increase their MAT by enhancing NADPH‐H2O2content and controlling chloroplast‐H2O2production during recovery, which enhances the expression of HS‐responsive genes and balances PCD levels, respectively.