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感染了……致病变种的感病和抗病品种的无标记定量蛋白质组学分析

Label-Free Quantitative Proteomics Analysis in Susceptible and Resistant Cultivars Infected with pv. .

作者信息

Islam Md Tabibul, Lee Bok-Rye, La Van Hien, Bae Dong-Won, Jung Woo-Jin, Kim Tae-Hwan

机构信息

Department of Animal Science, Institute of Agricultural Science and Technology, College of Agriculture & Life Science, Chonnam National University, Gwangju 61186, Korea.

Alson H. Smith Jr. Agricultural Research and Extension Center, School of Plant and Environmental Sciences, Virginia Tech, Winchester, VA 22602, USA.

出版信息

Microorganisms. 2021 Jan 27;9(2):253. doi: 10.3390/microorganisms9020253.

DOI:10.3390/microorganisms9020253
PMID:33513868
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7911590/
Abstract

Black rot, caused by pv. (), is the main disease of cruciferous vegetables. To characterize the resistance mechanism in the - pathosystem, -responsive proteins in susceptible (cv. Mosa) and resistant (cv. Capitol) cultivars were investigated using gel-free quantitative proteomics and analysis of gene expression. This allowed us to identify 158 and 163 differentially expressed proteins following infection in cv. Mosa and cv. Capitol, respectively, and to classify them into five major categories including antioxidative systems, proteolysis, photosynthesis, redox, and innate immunity. All proteins involved in protein degradation such as the protease complex, proteasome subunits, and ATP-dependent Clp protease proteolytic subunits, were upregulated only in cv. Mosa, in which higher hydrogen peroxide accumulation concurred with upregulated superoxide dismutase. In cv. Capitol, photosystem II (PS II)-related proteins were downregulated (excepting PS II 22 kDa), whereas the PS I proteins, ATP synthase, and ferredoxin-NADP reductase, were upregulated. For redox-related proteins, upregulation of thioredoxin, 2-cys peroxiredoxin, and glutathione S-transferase occurred in cv. Capitol, consistent with higher NADH-, ascorbate-, and glutathione-based reducing potential, whereas the proteins involved in the C oxidative cycle and glycolysis were highly activated in cv. Mosa. Most innate immunity-related proteins, including zinc finger domain (ZFD)-containing protein, glycine-rich RNA-binding protein (GRP) and mitochondrial outer membrane porin, were highly enhanced in cv. Capitol, concomitant with enhanced expression of and genes. Distinguishable differences in the protein profile between the two cultivars deserves higher importance for breeding programs and understanding of disease resistance in the - pathosystem.

摘要

由野油菜黄单胞菌致病变种(Xanthomonas campestris pv. campestris)引起的黑腐病是十字花科蔬菜的主要病害。为了阐明甘蓝-野油菜黄单胞菌致病型(Xanthomonas campestris pv. campestris)互作体系中的抗性机制,利用无胶定量蛋白质组学和基因表达分析,对感病品种(摩莎(cv. Mosa))和抗病品种(国会山(cv. Capitol))中与Xcc响应相关的蛋白质进行了研究。这使我们分别鉴定出了摩莎品种和国会山品种在接种Xcc后158个和163个差异表达蛋白,并将它们分为抗氧化系统、蛋白水解、光合作用、氧化还原和先天免疫五大类。所有参与蛋白质降解的蛋白质,如蛋白酶复合体、蛋白酶体亚基和ATP依赖的Clp蛋白酶水解亚基,仅在摩莎品种中上调,该品种中过氧化氢积累量较高,同时超氧化物歧化酶也上调。在国会山品种中,光系统II(PS II)相关蛋白下调(除PS II 22 kDa蛋白外),而光系统I蛋白、ATP合酶和铁氧还蛋白-NADP还原酶上调。对于氧化还原相关蛋白,硫氧还蛋白、2-半胱氨酸过氧化物酶和谷胱甘肽S-转移酶在国会山品种中上调,这与较高的基于NADH、抗坏血酸和谷胱甘肽的还原电位一致,而参与C氧化循环和糖酵解的蛋白在摩莎品种中高度活化。大多数与先天免疫相关的蛋白,包括含锌指结构域(ZFD)的蛋白、富含甘氨酸的RNA结合蛋白(GRP)和线粒体外膜孔蛋白,在国会山品种中高度增强,同时伴随着病程相关蛋白(PR)基因和茉莉酸(JA)基因表达的增强。两个品种之间蛋白质谱的显著差异对于育种计划和理解甘蓝-野油菜黄单胞菌致病型互作体系中的抗病性具有重要意义。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d1f/7911590/dfffd7b86615/microorganisms-09-00253-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d1f/7911590/a79393d9eca8/microorganisms-09-00253-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d1f/7911590/fb188b34d065/microorganisms-09-00253-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d1f/7911590/79ba8f3a76f9/microorganisms-09-00253-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d1f/7911590/9a2dbcd6f4db/microorganisms-09-00253-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d1f/7911590/bb02bbfaecd5/microorganisms-09-00253-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d1f/7911590/9921c69ed3f3/microorganisms-09-00253-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d1f/7911590/501f9068dcf1/microorganisms-09-00253-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d1f/7911590/dfffd7b86615/microorganisms-09-00253-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d1f/7911590/a79393d9eca8/microorganisms-09-00253-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d1f/7911590/fb188b34d065/microorganisms-09-00253-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d1f/7911590/79ba8f3a76f9/microorganisms-09-00253-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d1f/7911590/9a2dbcd6f4db/microorganisms-09-00253-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d1f/7911590/bb02bbfaecd5/microorganisms-09-00253-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d1f/7911590/9921c69ed3f3/microorganisms-09-00253-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d1f/7911590/501f9068dcf1/microorganisms-09-00253-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d1f/7911590/dfffd7b86615/microorganisms-09-00253-g008.jpg

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