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过氧化氢通过增强脯氨酸积累缓解盐胁迫对小麦幼苗的伤害。

Hydrogen peroxide alleviates salinity-induced damage through enhancing proline accumulation in wheat seedlings.

机构信息

MOE Key Laboratory of Environment Remediation and Ecological Health, College of Natural Resource and Environmental Sciences, Zhejiang University, Hangzhou, 310058, China.

出版信息

Plant Cell Rep. 2020 May;39(5):567-575. doi: 10.1007/s00299-020-02513-3. Epub 2020 Feb 6.

Abstract

NADPH oxidase-mediated HO maintains proline concentration under NaCl stress through regulating its biosynthesis and degradation, conferring salt tolerance to wheat plants. Considerable attention has been paid to the specific role of hydrogen peroxide (HO) in plant stress responses. Here, using microscopic, pharmacological and biochemical approaches, we explored HO production and its roles in redox control under salt stress in wheat roots. Exogenous HO pretreatment decreased salt-induced lipid peroxidation, while increased proline content in wheat roots. Salt stress led to a transient increase in NADPH oxidase activity accompanied by accumulation of HO and proline in roots. The elevated proline accumulation in the presence of NaCl was significantly suppressed by diphenyleneiodonium, an inhibitor of NADPH oxidase, and dimethylthiourea, a scavenger of HO. The rate-limiting enzyme involved in proline biosynthesis, Δ-pyrroline-5-carboxylate synthetase (P5CS), was induced by NaCl, whereas the house-keeping enzyme in proline degradation, proline dehydrogenase (ProDH), was inhibited. After 6 h, the activity of P5CS increased by 1.5-fold, whereas ProDH decreased by 13.9%. The levels of these enzymes, however, were restored by NADPH oxidase inhibitor or HO scavenger. After treatment with HO, the effects of diphenyleneiodonium and or dimethylthiourea on proline content and activities of P5CS and ProDH were reversed. These results suggested that NADPH oxidase-mediated HO alleviates oxidative damage induced by salt stress through regulating proline biosynthesis and degradation.

摘要

NADPH 氧化酶介导线粒体 HO 通过调节脯氨酸的生物合成和降解来维持 NaCl 胁迫下脯氨酸的浓度,从而赋予小麦植株耐盐性。人们对植物胁迫响应中过氧化氢(HO)的特定作用给予了相当大的关注。在这里,我们使用显微镜、药理学和生物化学方法,研究了 HO 的产生及其在小麦根中盐胁迫下氧化还原调控中的作用。外源性 HO 预处理可降低盐诱导的脂质过氧化,同时增加小麦根中的脯氨酸含量。盐胁迫导致 NADPH 氧化酶活性短暂增加,伴随着根中 HO 和脯氨酸的积累。NADPH 氧化酶抑制剂二苯并碘二酮和 HO 清除剂二甲基硫脲显著抑制 NaCl 存在时脯氨酸的积累。脯氨酸生物合成的限速酶Δ-吡咯啉-5-羧酸合成酶(P5CS)被 NaCl 诱导,而脯氨酸降解的管家酶脯氨酸脱氢酶(ProDH)受到抑制。6 小时后,P5CS 的活性增加了 1.5 倍,而 ProDH 降低了 13.9%。然而,这些酶的水平可以通过 NADPH 氧化酶抑制剂或 HO 清除剂恢复。用 HO 处理后,二苯并碘二酮和/或二甲基硫脲对脯氨酸含量以及 P5CS 和 ProDH 活性的影响被逆转。这些结果表明,NADPH 氧化酶介导线粒体 HO 通过调节脯氨酸的生物合成和降解来缓解盐胁迫引起的氧化损伤。

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