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      Tea plant ( Camellia sinensis) lipid metabolism pathway modulated by tea field microbe ( Colletotrichum camelliae) to promote disease

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      , , , ,
      Horticulture Research
      Oxford University Press

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          Abstract

          Tea is one of the most popular healthy and non-alcoholic beverages worldwide. Tea anthracnose is a disease in tea mature leaves and ultimately affects yield and quality. Colletotrichum camelliae is a dominant fungal pathogen in the tea field that infects tea plants in China. The pathogenic factors of fungus and the susceptible factors in the tea plant are not known. In this work, we performed molecular and genetic studies to observe a cerato-platanin protein CcCp1 from C. camelliae, which played a key role in fungal pathogenicity. △ CcCp1 mutants lost fungal virulence and reduced the ability to produce conidia. Transcriptome and metabolome were then performed and analysed in tea-susceptible and tea-resistant cultivars, Longjing 43 and Zhongcha 108, upon C. camelliae wild-type CCA and △ CcCp1 infection, respectively. The differentially expressed genes and the differentially accumulated metabolites in tea plants were clearly overrepresented such as linolenic acid and linoleic acid metabolism, glycerophospholipid metabolism, phenylalanine biosynthesis and metabolism, biosynthesis of flavonoid, flavone and flavonol etc. In particular, the accumulation of jasmonic acid was significantly increased in the susceptible cultivar Longjing 43 upon CCA infection, in the fungal CcCp1 protein dependent manner, suggesting the compound involved in regulating fungal infection. In addition, other metabolites in the glycerophospholipid and phenylalanine pathway were observed in the resistant cultivar Zhongcha 108 upon fungal treatment, suggesting their potential role in defense response. Taken together, this work indicated C. camelliae CcCp1 affected the tea plant lipid metabolism pathway to promote disease while the lost function of CcCp1 mutants altered the fungal virulence and plant response.

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          Many plant-associated microbes are pathogens that impair plant growth and reproduction. Plants respond to infection using a two-branched innate immune system. The first branch recognizes and responds to molecules common to many classes of microbes, including non-pathogens. The second responds to pathogen virulence factors, either directly or through their effects on host targets. These plant immune systems, and the pathogen molecules to which they respond, provide extraordinary insights into molecular recognition, cell biology and evolution across biological kingdoms. A detailed understanding of plant immune function will underpin crop improvement for food, fibre and biofuels production.
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              It has been suggested that effective defense against biotrophic pathogens is largely due to programmed cell death in the host, and to associated activation of defense responses regulated by the salicylic acid-dependent pathway. In contrast, necrotrophic pathogens benefit from host cell death, so they are not limited by cell death and salicylic acid-dependent defenses, but rather by a different set of defense responses activated by jasmonic acid and ethylene signaling. This review summarizes results from Arabidopsis-pathogen systems regarding the contributions of various defense responses to resistance to several biotrophic and necrotrophic pathogens. While the model above seems generally correct, there are exceptions and additional complexities.
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                Author and article information

                Contributors
                Journal
                Hortic Res
                Hortic Res
                hr
                Horticulture Research
                Oxford University Press
                2662-6810
                2052-7276
                April 2023
                21 February 2023
                21 February 2023
                : 10
                : 4
                : uhad028
                Affiliations
                Laboratory of Tea and Medicinal Plant Biology, College of Plant Sciences, Jilin University , Changchun 130062, China
                Laboratory of Molecular Plant Pathology, College of Plant Sciences, Jilin University , Changchun 130062, China
                Laboratory of Tea and Medicinal Plant Biology, College of Plant Sciences, Jilin University , Changchun 130062, China
                Laboratory of Molecular Plant Pathology, College of Plant Sciences, Jilin University , Changchun 130062, China
                Laboratory of Tea and Medicinal Plant Biology, College of Plant Sciences, Jilin University , Changchun 130062, China
                Laboratory of Molecular Plant Pathology, College of Plant Sciences, Jilin University , Changchun 130062, China
                Guangdong Provincial Key Laboratory of Tea Plant Resources Innovation and Utilization, Guangdong Academy of Agricultural Sciences Tea Research Institute , Guangzhou 510640, China
                Laboratory of Tea and Medicinal Plant Biology, College of Plant Sciences, Jilin University , Changchun 130062, China
                Laboratory of Molecular Plant Pathology, College of Plant Sciences, Jilin University , Changchun 130062, China
                Author notes
                Corresponding author. E-mail: shouan@ 123456jlu.edu.cn
                Article
                uhad028
                10.1093/hr/uhad028
                10117433
                37090093
                662efa96-fb0c-4c73-81bb-5eeb322bdb53
                © The Author(s) 2023. Published by Oxford University Press on behalf of Nanjing Agricultural University.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 27 August 2022
                : 13 February 2023
                : 01 April 2023
                Page count
                Pages: 28
                Categories
                Article
                AcademicSubjects/SCI01140

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