Quantitative proteomics analysis reveals that S-nitrosoglutathione reductase (GSNOR) and nitric oxide signaling enhance poplar defense against chilling stress
Quantitative proteomics analysis reveals that S-nitrosoglutathione reductase (GSNOR) and nitric oxide signaling enhance poplar defense against chilling stress
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DOI：
10.1007/s00425-015-2374-5
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发表时间：
2015-12-01
期刊：
影响因子：
4.3
通讯作者：
Shi, Jisen
中科院分区：
文献类型：
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作者：
Cheng, Tielong;Chen, Jinhui;Shi, Jisen
NO是通过抗氧化酶活性和蛋白质S-亚硝基化修饰来增强杨树对寒冷胁迫耐受性的重要信号，NO信号还受到S-亚硝基谷胱甘肽还原酶和硝酸盐还原酶的严格控制，以避免活性氮的过度积累。杨树（Populus trichocarpa）是快速生长的木本植物，具有两种特性： 生态和经济价值；然而，人们对杨树适应环境胁迫的机制知之甚少。在本研究中，我们使用同量异位标签进行相对和绝对定量蛋白质组学方法来表征杨树对冷胁迫的反应。我们鉴定了 114 种蛋白质，这些蛋白质在暴露于冷胁迫的植物中存在差异表达。特别是，一些蛋白质参与活性氧（ROS）和活性氮（RNS）代谢。进一步的生理分析表明，一氧化氮（NO）信号激活了一系列下游防御反应。我们进一步证明，NO 激活抗氧化酶活性和 S-亚硝基谷胱甘肽还原酶 (GSNOR) 活性，从而降低 ROS 和 RNS 毒性，从而增强杨树对冷胁迫的耐受性。抑制NO积累或GSNOR活性加剧了杨树叶片的冷害。此外，我们的结果表明，RNS 可以通过 S-亚硝基化抑制 GSNOR 和 NO 硝酸还原酶 (NR) 的活性，从而通过调节抗坏血酸过氧化物酶蛋白的 S-亚硝基化来微调 NO 信号并调节 ROS 水平。因此，我们的数据表明，NO 信号传导激活多种途径，增强杨树对冷胁迫的耐受性，并且 NO 信号传导通过 S-亚硝基化的蛋白质翻译后修饰受到严格控制。
NO acts as the essential signal to enhance poplar tolerance to chilling stress via antioxidant enzyme activities and protein S -nitrosylation modification, NO signal is also strictly controlled by S -nitrosoglutathione reductase and nitrate reductase to avoid the over-accumulation of reactive nitrogen species.Poplar (Populus trichocarpa) are fast growing woody plants with both ecological and economic value; however, the mechanisms by which poplar adapts to environmental stress are poorly understood. In this study, we used isobaric tags for relative and absolute quantification proteomic approach to characterize the response of poplar exposed to cold stress. We identified 114 proteins that were differentially expressed in plants exposed to cold stress. In particular, some of the proteins are involved in reactive oxygen species (ROS) and reactive nitrogen species (RNS) metabolism. Further physiological analysis showed that nitric oxide (NO) signaling activated a series of downstream defense responses. We further demonstrated that NO activated antioxidant enzyme activities and S-nitrosoglutathione reductase (GSNOR) activities, which would reduce ROS and RNS toxicity and thereby enhance poplar tolerance to cold stress. Suppressing NO accumulation or GSNOR activity aggravated cold damage to poplar leaves. Moreover, our results showed that RNS can suppress the activities of GSNOR and NO nitrate reductase (NR) by S-nitrosylation to fine-tune the NO signal and modulate ROS levels by modulating the S-nitrosylation of ascorbate peroxidase protein. Hence, our data demonstrate that NO signaling activates multiple pathways that enhance poplar tolerances to cold stress, and that NO signaling is strictly controlled through protein post-translational modification by S-nitrosylation.