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首页> 外文期刊>Journal of Experimental Botany >Roles of NIA/NR/NOA1-dependent nitric oxide production and HY1 expression in the modulation of Arabidopsis salt tolerance.
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Roles of NIA/NR/NOA1-dependent nitric oxide production and HY1 expression in the modulation of Arabidopsis salt tolerance.

机译：NIA / NR / NOA1依赖性一氧化氮产生和HY1表达在拟南芥耐盐性调节中的作用。

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摘要

Despite substantial evidence on the separate roles of Arabidopsis nitric oxide-associated 1 (NOA1)-associated nitric oxide (NO) production and haem oxygenase 1 (HY1) expression in salt tolerance, their integrative signalling pathway remains largely unknown. To fill this knowledge gap, the interaction network among nitrate reductase (NIA/NR)- and NOA1-dependent NO production and HY1 expression was studied at the genetic and molecular levels. Upon salinity stress, the majority of NO production was attributed to NIA/NR/NOA1. Further evidence confirmed that HY1 mutant hy1-100, nia1/2oa1, and nia1/2oa1/hy1-100 mutants exhibited progressive salt hypersensitivity, all of which were significantly rescued by three NO-releasing compounds. The salinity-tolerant phenotype and the stronger NO production in gain-of-function mutant of HY1 were also blocked by the NO synthetic inhibitor and scavenger. Although NO- or HY1-deficient mutants showed a compensatory mode of upregulation of HY1 or slightly increased NO production, respectively, during 2 d of salt treatment, downregulation of ZAT10/12-mediated antioxidant gene expression (cAPX1/2 and FSD1) was observed after 7 d of treatment. The hypersensitive phenotypes and stress-related genes expression profiles were differentially rescued or blocked by the application of NO- (in particular) or carbon monoxide (CO)-releasing compounds, showing a synergistic mode. Similar reciprocal responses were observed in the nia1/2oa1/hy1-100 quadruple mutant, with the NO-releasing compounds exhibit the maximal rescuing responses. Overall, the findings present the combination of compensatory and synergistic modes, linking NIA/NR/NOA1-dependent NO production and HY1 expression in the modulation of plant salt tolerance.
机译：尽管有大量证据证明拟南芥一氧化氮相关1（NOA1）相关的一氧化氮（NO）产生和血红素加氧酶1（HY1）在盐耐受性中的独立作用，但它们的整合信号传导途径仍然很大程度上未知。为了填补这一知识空白，在遗传和分子水平上研究了硝酸还原酶（NIA / NR）和依赖NOA1的NO产生与HY1表达之间的相互作用网络。在盐分胁迫下，NO的产生主要归因于NIA / NR / NOA1。进一步的证据证实，HY1突变体hy1-100，nia1 / 2 / noa1和nia1 / 2 / noa1 / hy1-100突变体表现出进行性盐超敏性，所有这些均通过三种NO释放化合物得到了显着拯救。 NO合成抑制剂和清除剂也阻断了耐盐性表型和HY1功能获得突变体中较强的NO产生。尽管缺乏NO或HY1的突变体分别显示出HY1上调的补偿模式或NO生成略有增加，但在盐处理2天期间，观察到ZAT10 / 12介导的抗氧化剂基因表达（cAPX1 / 2和FSD1）下调治疗7天后。超敏性表型和应激相关基因的表达谱通过应用NO-（尤其是）或释放一氧化碳（CO）的化合物进行差异拯救或阻断，表现出协同模式。在nia1 / 2 / noa1 / hy1-100四重突变体中观察到类似的相互反应，其中释放NO的化合物表现出最大的拯救反应。总的来说，这些发现提出了补偿模式和协同模式的结合，将NIA / NR / NOA1依赖性NO的产生与HY1的表达联系起来，从而调节了植物的耐盐性。

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