柑橘疫霉菌(Geotrichum citri-aurantii)的关键致病因子 GcSP2 在破坏柑橘新陈代谢和免疫方面发挥着重要作用

IF 6.4 1区 农林科学 Q1 AGRONOMY
Rong Liu , Haoxiang Zheng , Di Wang , Haijue Zhang , Yan Wu , Xue Li , Zhengfeng Liu , QingJun Kong , Xueyan Ren
{"title":"柑橘疫霉菌(Geotrichum citri-aurantii)的关键致病因子 GcSP2 在破坏柑橘新陈代谢和免疫方面发挥着重要作用","authors":"Rong Liu ,&nbsp;Haoxiang Zheng ,&nbsp;Di Wang ,&nbsp;Haijue Zhang ,&nbsp;Yan Wu ,&nbsp;Xue Li ,&nbsp;Zhengfeng Liu ,&nbsp;QingJun Kong ,&nbsp;Xueyan Ren","doi":"10.1016/j.postharvbio.2024.113253","DOIUrl":null,"url":null,"abstract":"<div><div>The pathogen <em>Geotrichum citri-aurantii</em> (<em>G. citri-aurantii</em>) causes postharvest sour rot disease in citrus fruits worldwide, severely impacting citrus economic value. However, the pathogenic mechanisms of this fungus remain inadequately understood. Here, we identified 15 candidate effector proteins from <em>G. citri-aurantii</em> genome, of which five were highly expressed during infection and were capable of suppressing BAX-induced cell death, indicating their role in inhibiting plant immunity. Gene expression analysis showed that these five effector proteins primarily induced the upregulation of pattern-triggered immunity (PTI)-related gene expression. Diaminobenzidine (DAB) staining results indicated that only <em>GcSP2</em> triggered reactive oxygen species (ROS) burst. Notably, <em>GcSP2</em> contains a known carbohydrate-binding module 1 (CBM1) domain and exhibits low overall conservation. Gene knockout experiments revealed that the absence of <em>GcSP2</em> delayed disease onset by 1–2 days and significantly reduced lesion size, establishing it as a key pathogenic factor. Assessments of total phenols, flavonoids, and pathogenesis-related protein expression indicated that <em>GcSP2</em> significantly affects citrus metabolism at 72 hours post-infection.</div></div>","PeriodicalId":20328,"journal":{"name":"Postharvest Biology and Technology","volume":"219 ","pages":"Article 113253"},"PeriodicalIF":6.4000,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"The key pathogenic factor GcSP2 of Geotrichum citri-aurantii plays an important role in disrupting citrus metabolism and immunity\",\"authors\":\"Rong Liu ,&nbsp;Haoxiang Zheng ,&nbsp;Di Wang ,&nbsp;Haijue Zhang ,&nbsp;Yan Wu ,&nbsp;Xue Li ,&nbsp;Zhengfeng Liu ,&nbsp;QingJun Kong ,&nbsp;Xueyan Ren\",\"doi\":\"10.1016/j.postharvbio.2024.113253\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>The pathogen <em>Geotrichum citri-aurantii</em> (<em>G. citri-aurantii</em>) causes postharvest sour rot disease in citrus fruits worldwide, severely impacting citrus economic value. However, the pathogenic mechanisms of this fungus remain inadequately understood. Here, we identified 15 candidate effector proteins from <em>G. citri-aurantii</em> genome, of which five were highly expressed during infection and were capable of suppressing BAX-induced cell death, indicating their role in inhibiting plant immunity. Gene expression analysis showed that these five effector proteins primarily induced the upregulation of pattern-triggered immunity (PTI)-related gene expression. Diaminobenzidine (DAB) staining results indicated that only <em>GcSP2</em> triggered reactive oxygen species (ROS) burst. Notably, <em>GcSP2</em> contains a known carbohydrate-binding module 1 (CBM1) domain and exhibits low overall conservation. Gene knockout experiments revealed that the absence of <em>GcSP2</em> delayed disease onset by 1–2 days and significantly reduced lesion size, establishing it as a key pathogenic factor. Assessments of total phenols, flavonoids, and pathogenesis-related protein expression indicated that <em>GcSP2</em> significantly affects citrus metabolism at 72 hours post-infection.</div></div>\",\"PeriodicalId\":20328,\"journal\":{\"name\":\"Postharvest Biology and Technology\",\"volume\":\"219 \",\"pages\":\"Article 113253\"},\"PeriodicalIF\":6.4000,\"publicationDate\":\"2024-10-18\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Postharvest Biology and Technology\",\"FirstCategoryId\":\"97\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0925521424004988\",\"RegionNum\":1,\"RegionCategory\":\"农林科学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"AGRONOMY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Postharvest Biology and Technology","FirstCategoryId":"97","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0925521424004988","RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"AGRONOMY","Score":null,"Total":0}
引用次数: 0

摘要

柑橘酸腐病病原菌(Geotrichum citri-aurantii,G. citri-aurantii)在全球范围内引起柑橘采后酸腐病,严重影响柑橘的经济价值。然而,人们对这种真菌的致病机制仍然了解不足。在此,我们从 G. citri-aurantii 基因组中发现了 15 个候选效应蛋白,其中 5 个在感染过程中高表达,并能抑制 BAX 诱导的细胞死亡,表明它们在抑制植物免疫中的作用。基因表达分析表明,这五种效应蛋白主要诱导模式触发免疫(PTI)相关基因表达上调。二氨基联苯胺(DAB)染色结果表明,只有 GcSP2 能引发活性氧(ROS)猝灭。值得注意的是,GcSP2 含有一个已知的碳水化合物结合模块 1(CBM1)结构域,且整体保存率较低。基因敲除实验表明,GcSP2 的缺失会使发病时间延迟 1-2 天,并显著缩小病变范围,从而确定它是一个关键的致病因素。对总酚、类黄酮和致病相关蛋白表达的评估表明,GcSP2 对柑橘感染后 72 小时的新陈代谢有显著影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The key pathogenic factor GcSP2 of Geotrichum citri-aurantii plays an important role in disrupting citrus metabolism and immunity
The pathogen Geotrichum citri-aurantii (G. citri-aurantii) causes postharvest sour rot disease in citrus fruits worldwide, severely impacting citrus economic value. However, the pathogenic mechanisms of this fungus remain inadequately understood. Here, we identified 15 candidate effector proteins from G. citri-aurantii genome, of which five were highly expressed during infection and were capable of suppressing BAX-induced cell death, indicating their role in inhibiting plant immunity. Gene expression analysis showed that these five effector proteins primarily induced the upregulation of pattern-triggered immunity (PTI)-related gene expression. Diaminobenzidine (DAB) staining results indicated that only GcSP2 triggered reactive oxygen species (ROS) burst. Notably, GcSP2 contains a known carbohydrate-binding module 1 (CBM1) domain and exhibits low overall conservation. Gene knockout experiments revealed that the absence of GcSP2 delayed disease onset by 1–2 days and significantly reduced lesion size, establishing it as a key pathogenic factor. Assessments of total phenols, flavonoids, and pathogenesis-related protein expression indicated that GcSP2 significantly affects citrus metabolism at 72 hours post-infection.
求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Postharvest Biology and Technology
Postharvest Biology and Technology 农林科学-农艺学
CiteScore
12.00
自引率
11.40%
发文量
309
审稿时长
38 days
期刊介绍: The journal is devoted exclusively to the publication of original papers, review articles and frontiers articles on biological and technological postharvest research. This includes the areas of postharvest storage, treatments and underpinning mechanisms, quality evaluation, packaging, handling and distribution of fresh horticultural crops including fruit, vegetables, flowers and nuts, but excluding grains, seeds and forages. Papers reporting novel insights from fundamental and interdisciplinary research will be particularly encouraged. These disciplines include systems biology, bioinformatics, entomology, plant physiology, plant pathology, (bio)chemistry, engineering, modelling, and technologies for nondestructive testing. Manuscripts on fresh food crops that will be further processed after postharvest storage, or on food processes beyond refrigeration, packaging and minimal processing will not be considered.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信