Glutathione signaling acts through NPR1-dependent SA-mediated pathway to mitigate biotic stress
Glutathione signaling acts through NPR1-dependent SA-mediated pathway to mitigate biotic stress
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DOI：
10.4161/psb.6.4.15402
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发表时间：
2011-01-01
影响因子：
2.9
通讯作者：
Chattopadhyay, Sharmila
中科院分区：
文献类型：
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作者：
Ghanta, Srijani;Bhattacharyya, Dipto;Chattopadhyay, Sharmila
谷胱甘肽（GSH）是一种多功能的抗氧化分子，但近年来又发现了它在植物防御信号转导中的新作用。过去三十年的研究表明，GSH在植物的病原体防御中起作用，但其机制尚未完全阐明。我们最近发现，GSH作为一种信号分子，通过PR基因非表达子1（NPR 1）依赖的水杨酸（SA）介导的途径减轻生物胁迫。研究发现，GSH水平提高的转基因烟草（NtGB株系）合成更多的SA，能够提高NPR 1依赖的SA介导途径基因的表达，并能抵抗活体营养型病原菌Pseudomonaseringae，许多SA相关蛋白表达上调。这些结果收集了GSH对抗生物胁迫机制的实验证据。在继续与我们以前的调查，我们在这里表明，谷胱甘肽S-转移酶（GST）的表达，NPR 1独立SA介导的基因是不变的，在转基因烟草与增强水平的GSH相比，野生型植物。此外，转基因植物几乎不抵抗灰葡萄孢，坏死营养型病原体。SA处理导致病程相关蛋白基因（PR 1）和PR 4的表达水平增强，而短链脱氢酶/还原酶家族蛋白（SDRLP）和丙二烯氧化物合酶（AOS）则相反。这些数据提供了重要的洞察参与NPR 1依赖SA介导的途径，在减轻生物胁迫的GSH。
Glutathione (GSH) has widely been known to be a multifunctional molecule especially as an antioxidant up until now, but has found a new role in plant defense signaling. Research from the past three decades indicate that GSH is a player in pathogen defense in plants, but the mechanism underlying this has not been elucidated fully. We have recently shown that GSH acts as a signaling molecule and mitigates biotic stress through non-expressor of PR genes 1 (NPR1)-dependent salicylic acid (SA)-mediated pathway. Transgenic tobacco with enhanced level of GSH (NtGB lines) was found to synthesize more SA, was capable of enhanced expression of genes belonging to NPR1-dependent SA-mediated pathway, were resistant to Pseudomonas syringae, the biotrophic pathogen and many SA-related proteins were upregulated. These results gathered experimental evidence on the mechanism through which GSH combats biotic stress. In continuation with our previous investigation we show here that the expression of glutathione S-transferase (GST), the NPR1-independent SA-mediated gene was unchanged in transgenic tobacco with enhanced level of GSH as compared to wild-type plants. Additionally, the transgenic plants were barely resistant to Botrytis cinerea, the necrotrophic pathogen. SA-treatment led to enhanced level of expression of pathogenesis-related protein gene (PR1) and PR4 as against short-chain dehydrogenase/reductase family protein (SDRLP) and allene oxide synthase (AOS). These data provided significant insight into the involvement of GSH in NPR1-dependent SA-mediated pathway in mitigating biotic stress.