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一个小麦超氧化物歧化酶基因TaSOD2通过促进NADPH氧化酶活性调节氧化还原稳态来增强耐盐性。

A wheat superoxide dismutase gene TaSOD2 enhances salt resistance through modulating redox homeostasis by promoting NADPH oxidase activity.

作者信息

Wang Mengcheng, Zhao Xin, Xiao Zhen, Yin Xunhao, Xing Tian, Xia Guangmin

机构信息

The Key Laboratory of Plant Cell Engineering and Germplasm Innovation, Ministry of Education, School of Life Science, Shandong University, 27 Shandanan Road, Jinan, 250100, Shandong, China.

出版信息

Plant Mol Biol. 2016 May;91(1-2):115-30. doi: 10.1007/s11103-016-0446-y. Epub 2016 Feb 11.

Abstract

Superoxide dismutase (SOD) is believed to enhance abiotic stress resistance by converting superoxide radical (O2 (-)) to H2O2 to lower ROS level and maintain redox homeostasis. ROS level is controlled via biphasic machinery of ROS production and scavenging. However, whether the role of SOD in abiotic stress resistance is achieved through influencing the biophasic machinery is not well documented. Here, we identified a wheat copper-zinc (Cu/Zn) SOD gene, TaSOD2, who was responsive to NaCl and H2O2. TaSOD2 overexpression in wheat and Arabidopsis elevated SOD activities, and enhanced the resistance to salt and oxidative stress. TaSOD2 overexpression reduced H2O2 level but accelerated O2 (-) accumulation. Further, it improved the activities of H2O2 metabolic enzymes, elevated the activity of O2 (-) producer NADPH oxidase (NOX), and promoted the transcription of NOX encoding genes. The inhibition of NOX activity and the mutation of NOX encoding genes both abolished the salt resistance of TaSOD2 overexpression lines. These data indicate that Cu/Zn SOD enhances salt resistance, which is accomplished through modulating redox homeostasis via promoting NOX activity.

摘要

超氧化物歧化酶(SOD)被认为通过将超氧阴离子自由基(O2(-))转化为H2O2来降低活性氧水平并维持氧化还原稳态,从而增强非生物胁迫抗性。活性氧水平通过活性氧产生和清除的双相机制来控制。然而,SOD在非生物胁迫抗性中的作用是否通过影响双相机制来实现,目前尚无充分的文献记载。在此,我们鉴定了一个小麦铜锌(Cu/Zn)SOD基因TaSOD2,它对NaCl和H2O2有响应。TaSOD2在小麦和拟南芥中的过表达提高了SOD活性,并增强了对盐和氧化胁迫的抗性。TaSOD2过表达降低了H2O2水平,但加速了O2(-)的积累。此外,它提高了H2O2代谢酶的活性,提高了O2(-)产生者NADPH氧化酶(NOX)的活性,并促进了NOX编码基因的转录。抑制NOX活性和突变NOX编码基因均消除了TaSOD2过表达系的耐盐性。这些数据表明,Cu/Zn SOD通过促进NOX活性调节氧化还原稳态来增强耐盐性。

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