铜绿假单胞菌代谢物诱导蝴蝶兰耐冷胁迫和抗软腐病的共同细胞事件

Huey-Wen Chuang, T. Tseng, Hsin-Yi Hsieh, T. Kao, Guanjun Chen
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引用次数: 1

摘要

微生物代谢产物诱导多种植物生理反应。在这项研究中,铜绿假单胞菌Y1菌株被证明产生的代谢物具有高的金属螯合能力和中等的还原活性。Y1代谢物(Y1M)处理提高了蝴蝶兰碳水化合物和木质素含量以及抗氧化酶和苯丙氨酸解氨酶(PAL)活性。Y1M处理通过减少10°C生长环境下丙二醛(MDA)积累和电解质泄漏,提高了对冷胁迫(10°C)的耐受性,增强了对菊花Erwinia引起的细菌性软腐病的抗病性。蛋白质分析表明,在Y1M处理下,抗氧化酶,如过氧化氢酶(CAT)和抗坏血酸过氧化物酶(APX)的蛋白质水平;发病相关(PR)蛋白,如PR-2和PR-3;脂氧合酶1 (LOX1)升高。转录组分析表明,Y1M增加的转录与miRNA介导的缺铁反应、活性氧(ROS)稳态调节和茉莉酸(JA)生物合成/感知相关。与诱导防御反应相关的基因群,包括模式触发免疫(PTI)、超敏反应(HR)、PR蛋白合成和胼胝质的形成,也在Y1M处理下增加。参与调节冷应激反应的转录因子,如c -重复结合因子1 (CBF1)和细胞强化因子,如MYB26的表达也有所增加。综上所述,Y1M可以激活与调节冷胁迫和细菌入侵共有的胁迫耐受性有关的细胞通路。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Common Cellular Events Implicated in the Regulation of Cold Stress Tolerance and Soft Rot Resistance Induced by Metabolites of Pseudomonas Aeruginosa in Phalaenopsis Orchids
Microbial metabolites induce diverse plant physiological responses. In this study, Pseudomonas aeruginosa strain Y1 was shown to produce metabolites exhibiting a high capacity for metal chelation and moderate reducing power activity. In Phalaenopsis orchids, treatments with Y1 metabolites (Y1M) increased the contents of carbohydrates and lignin and the activity of antioxidant enzymes and phenylalanine ammonia lyase (PAL). Y1M treatments increased the tolerance to cold stress (10°C) by reducing malondialdehyde (MDA) accumulation and electrolyte leakage in a 10°C growth environment and enhanced disease resistance against bacterial soft rot caused by Erwinia chrysanthemi. Protein analyses indicated that, in response to Y1M treatment, the protein levels of antioxidant enzymes, such as catalase (CAT) and ascorbate peroxidase (APX); pathogenesis-related (PR) proteins, such as PR-2 and PR-3; and lipoxygenase 1 (LOX1) were increased in Phalaenopsis orchids. Transcriptome analyses indicated that Y1M increased transcription associated with the iron-deficient response mediated by miRNA, the regulation of reactive oxygen species (ROS) homeostasis, and Jasmonic acid (JA) biosynthesis/perception. Gene groups associated with the induced defense response, including cellular events of pattern-triggered immunity (PTI), hypersensitive response (HR), synthesis of the PR protein, and callose formation, were also increased by the Y1M treatments. Transcription factors involved in regulating the cold stress response, such as C-repeat binding factor 1 (CBF1), and cell strengthening, such as MYB26, also had increased expression. In summary, Y1M can activate cellular pathways implicated in regulating stress tolerance shared by cold stress and bacterial invasion.
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