Exogenous L-Arginine Enhances Pathogenicity of Alternaria alternata on Kiwifruit by Regulating Metabolisms of Nitric Oxide, Polyamines, Reactive Oxygen Species (ROS), and Cell Wall Modification.

IF 4.2 2区 生物学 Q2 MICROBIOLOGY Journal of Fungi Pub Date : 2024-11-19 DOI:10.3390/jof10110801
Di Wang, Lingkui Meng, Haijue Zhang, Rong Liu, Yuhan Zhu, Xinyu Tan, Yan Wu, Qingchao Gao, Xueyan Ren, Qingjun Kong
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Abstract

Black spot, one of the major diseases of kiwifruit, is caused by Alternaria alternata. A comprehensive investigation into its pathogenicity mechanism is imperative in order to propose a targeted and effective control strategy. The effect of L-arginine on the pathogenicity of A. alternata and the underlying mechanisms were investigated. The results showed that treatment with 5 mM L-1 of L-arginine promoted spore germination and increased the colony diameter and lesion diameter of A. alternata in vivo and in vitro, which were 23.1% and 9.3% higher than that of the control, respectively. Exogenous L-arginine treatment also induced endogenous L-arginine and nitric oxide (NO) accumulation by activating nitric oxide synthase (NOS), arginine decarboxylase (ADC) and ornithine decarboxylase (ODC). In addition, exogenous L-arginine triggered an increase in reactive oxygen species (ROS) levels by activating the activity and inducing gene expression upregulation of NADPH oxidase. The hydrogen peroxide (H2O2) and superoxide anion (O2.-) levels were 15.9% and 2.2 times higher, respectively, than in the control group on the second day of L-arginine treatment. Meanwhile, antioxidant enzyme activities and gene expression levels were enhanced, including superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX), glutathione peroxidase (GPX), and glutathione reductase (GR). In addition, exogenous L-arginine stimulated cell wall-degrading enzymes in vivo and in vitro by activating gene expression. These results suggested that exogenous L-arginine promoted the pathogenicity of A. alternata by inducing the accumulation of polyamines, NO, and ROS, and by activating systems of antioxidants and cell wall-degrading enzymes. The present study not only revealed the mechanism by which low concentrations of L-arginine increase the pathogenicity of A. alternata, but also provided a theoretical basis for the exclusive and precise targeting of A. alternata in kiwifruit.

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外源性 L-精氨酸通过调节一氧化氮、多胺、活性氧(ROS)和细胞壁修饰的新陈代谢,增强交替孢霉对猕猴桃的致病性。
黑斑病是猕猴桃的主要病害之一,由 Alternaria alternata 引起。为了提出有针对性的有效防治策略,必须对其致病机理进行全面研究。本文研究了 L-精氨酸对交替丝核菌致病性的影响及其内在机制。结果表明,5 mM L-1的L-精氨酸处理可促进交替缠枝金龟子孢子的萌发,增加其体内和体外的菌落直径和病斑直径,分别比对照组高23.1%和9.3%。外源 L-精氨酸处理还能通过激活一氧化氮合酶(NOS)、精氨酸脱羧酶(ADC)和鸟氨酸脱羧酶(ODC),诱导内源性 L-精氨酸和一氧化氮(NO)的积累。此外,外源性 L-精氨酸通过激活 NADPH 氧化酶的活性和诱导基因表达上调,引发活性氧(ROS)水平的增加。L-精氨酸处理第二天,过氧化氢(H2O2)和超氧阴离子(O2.-)水平分别是对照组的 15.9% 和 2.2 倍。同时,抗氧化酶活性和基因表达水平也得到了提高,包括超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、抗坏血酸过氧化物酶(APX)、谷胱甘肽过氧化物酶(GPX)和谷胱甘肽还原酶(GR)。此外,外源性 L-精氨酸通过激活基因表达,刺激体内和体外的细胞壁降解酶。这些结果表明,外源 L-精氨酸通过诱导多胺、NO 和 ROS 的积累,以及激活抗氧化剂和细胞壁降解酶系统,促进了交替穗霉的致病性。本研究不仅揭示了低浓度 L-精氨酸增加交替穗霉致病性的机理,还为猕猴桃中交替穗霉的独家精准靶向治疗提供了理论依据。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Journal of Fungi
Journal of Fungi Medicine-Microbiology (medical)
CiteScore
6.70
自引率
14.90%
发文量
1151
审稿时长
11 weeks
期刊介绍: Journal of Fungi (ISSN 2309-608X) is an international, peer-reviewed scientific open access journal that provides an advanced forum for studies related to pathogenic fungi, fungal biology, and all other aspects of fungal research. The journal publishes reviews, regular research papers, and communications in quarterly issues. Our aim is to encourage scientists to publish their experimental and theoretical results in as much detail as possible. Therefore, there is no restriction on paper length. Full experimental details must be provided so that the results can be reproduced.
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