Melatonin delays leaf senescence of postharvest Chinese flowering cabbage through ROS homeostasis

文献类型： 外文期刊

第一作者： Tan, Xiao-li

作者： Tan, Xiao-li;Zhao, Ya-ting;Shan, Wei;Kuang, Jian-fei;Lu, Wang-jin;Chen, Jian-ye;Tan, Xiao-li;Zhao, Ya-ting;Shan, Wei;Kuang, Jian-fei;Lu, Wang-jin;Chen, Jian-ye;Su, Xin-guo;Tan, Xiao-li;Tao, Neng-guo;Lakshmanan, Prakash;Lakshmanan, Prakash;Lakshmanan, Prakash

作者机构：

关键词： Chinese flowering cabbage; Leaf senescence; Melatonin; ROS homeostasis

期刊名称：FOOD RESEARCH INTERNATIONAL （ 影响因子：6.475； 五年影响因子：6.508 ）

ISSN： 0963-9969

年卷期： 2020 年 138 卷

页码：

收录情况： SCI

摘要： Reactive oxygen species (ROS) trigger and accelerate leaf senescence. Melatonin, a low molecular compound with several biological functions in plants, is known to delay leaf senescence in different species, including Chinese flowering cabbage. However, the mechanism(s) underpinning melatonin-delayed leaf senescence remains unclear. Here, we found that melatonin lowered the expression of chlorophyll catabolic genes (BrPAO and BrSGR1) and senescence-associated genes (BrSAG12 and BrSEN4), decreased chlorophyll loss, minimized the alteration in Fv/Fm ratio and remarkably delayed senescence of Chinese flowering cabbage after harvest. Moreover, the over-accumulation of O-2(center dot-), hydrogen peroxide (H2O2) and malondialdehyde contents and the expression of respiratory burst oxidase homologues (RBOH) genes (BrRbohB, BrRbohC, BrRbohD, BrRbohD2 and BrRbohE) were significantly inhibited by melatonin treatment. Melatonin-treated cabbages also showed higher O-2(center dot-), OH center dot and DPPH radical scavenging capacity and enhanced activities of peroxidase (POD), superoxide dismutase (SOD) and their gene expressions. Up-regulation of key components of ascorbate-glutathione (AsA-GSH) cycle, the metabolic pathway that detoxify H2O2, was also observed in melatonin-treated cabbages. These findings suggest that melatonin-delayed postharvest leaf senescence of postharvest Chinese flowering cabbage may be mediated, at least in part, by maintaining ROS homeostasis through restraining RBOHs-catalyzed ROS production and enhancing the activity of ROS-scavenging system including major antioxidant enzymes and AsA-GSH cycle.

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