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血红素加氧酶-1 通过调节活性氧稳态与小麦的耐盐性有关。

Heme oxygenase-1 is associated with wheat salinity acclimation by modulating reactive oxygen species homeostasis.

机构信息

College of Life Sciences, Cooperative Demonstration Laboratory of Centrifuge Technique, Nanjing Agricultural University and Beckman Coulter Ltd. Co., Nanjing Agricultural University, China.

出版信息

J Integr Plant Biol. 2011 Aug;53(8):653-70. doi: 10.1111/j.1744-7909.2011.01052.x.

DOI:10.1111/j.1744-7909.2011.01052.x
PMID:21564546
Abstract

Heme oxygenase-1 (HO-1) has been recently identified as an endogenous signaling system in animals. In this study, HO-1 upregulation and its role in acquired salt tolerance (salinity acclimation) were investigated in wheat plants. We discovered that pretreatment with a low concentration of NaCl (25 mmol/L) not only led to the induction of HO-1 protein and gene expression, as well as enhanced HO activity, but also to a salinity acclimatory response thereafter. The effect is specific for HO-1, since the potent HO-1 inhibitor zinc protoporphyrin IX blocks the above cytoprotective actions, and the cytotoxic responses conferred by 200 mmol/L NaCl are reversed partially when HO-1 inducer hemin is added. Heme oxygenase catalytic product, carbon monoxide (CO) aqueous solution pretreatment, mimicked the salinity acclimatory responses. Meanwhile, the CO-triggered re-establishment of reactive oxygen species (ROS) homeostasis was mainly guaranteed by the induction of total and isozymatic activities, or corresponding transcripts of superoxide dismutase, ascorbate peroxidase, and cytosolic peroxidase (POD), as well as the downregulation of NADPH oxidase expression and cell-wall POD activity. A requirement of hydrogen peroxide homeostasis for HO-1-mediated salinity acclimation was also discovered. Taken together, the above results suggest that the upregulation of HO-1 expression was responsible for the observed salinity acclimation through the regulation of ROS homeostasis.

摘要

血红素加氧酶-1(HO-1)最近被鉴定为动物体内的一种内源性信号系统。在本研究中,研究了小麦植株中 HO-1 的上调及其在获得耐盐性(盐驯化)中的作用。我们发现,用低浓度的 NaCl(25mmol/L)预处理不仅导致 HO-1 蛋白和基因表达的诱导,以及 HO 活性的增强,而且随后还导致盐驯化反应。这种作用是 HO-1 特异的,因为有效的 HO-1 抑制剂锌原卟啉 IX 阻断了上述细胞保护作用,而当添加 HO-1 诱导剂血红素时,200mmol/L NaCl 赋予的细胞毒性反应部分逆转。血红素加氧酶催化产物一氧化碳(CO)水溶液预处理模拟了盐驯化反应。同时,CO 触发的活性氧(ROS)稳态的重新建立主要通过超氧化物歧化酶、抗坏血酸过氧化物酶和胞质过氧化物酶(POD)的总活性和同工酶活性或相应的转录物的诱导,以及 NADPH 氧化酶表达和细胞壁 POD 活性的下调来保证。还发现 HO-1 介导的盐驯化需要过氧化氢稳态。综上所述,上述结果表明,HO-1 表达的上调通过调节 ROS 稳态来负责观察到的盐驯化。

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