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      The early response during the interaction of fungal phytopathogen and host plant

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          Abstract

          Plants can be infected by a variety of pathogens, most of which can cause severe economic losses. The plants resist the invasion of pathogens via the innate or acquired immune system for surviving biotic stress. The associations between plants and pathogens are sophisticated beyond imaging and the interactions between them can occur at a very early stage after their touching each other. A number of researchers in the past decade have shown that many biochemical events appeared even as early as 5 min after their touching for plant disease resistance response. The early molecular interactions of plants and pathogens are likely to involve protein phosphorylation, ion fluxes, reactive oxygen species (ROS) and other signalling transduction. Here, we reviewed the recent progress in the study for molecular interaction response of fungal pathogens and host plant at the early infection stage, which included many economically important crop fungal pathogens such as cereal rust fungi, tomato Cladosporium fulvum, rice blast and so on. By dissecting the earlier infection stage of the diseases, the avirulent/virulent genes of pathogen or resistance genes of plant could be defined more clearly and accurately, which would undoubtedly facilitate fungal pathogenesis study and resistant crop breeding.

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          Plant pathogens and integrated defence responses to infection.

          Plants cannot move to escape environmental challenges. Biotic stresses result from a battery of potential pathogens: fungi, bacteria, nematodes and insects intercept the photosynthate produced by plants, and viruses use replication machinery at the host's expense. Plants, in turn, have evolved sophisticated mechanisms to perceive such attacks, and to translate that perception into an adaptive response. Here, we review the current knowledge of recognition-dependent disease resistance in plants. We include a few crucial concepts to compare and contrast plant innate immunity with that more commonly associated with animals. There are appreciable differences, but also surprising parallels.
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            Fungal effector proteins.

            It is accepted that most fungal avirulence genes encode virulence factors that are called effectors. Most fungal effectors are secreted, cysteine-rich proteins, and a role in virulence has been shown for a few of them, including Avr2 and Avr4 of Cladosporium fulvum, which inhibit plant cysteine proteases and protect chitin in fungal cell walls against plant chitinases, respectively. In resistant plants, effectors are directly or indirectly recognized by cognate resistance proteins that reside either inside the plant cell or on plasma membranes. Several secreted effectors function inside the host cell, but the uptake mechanism is not yet known. Variation observed among fungal effectors shows two types of selection that appear to relate to whether they interact directly or indirectly with their cognate resistance proteins. Direct interactions seem to favor point mutations in effector genes, leading to amino acid substitutions, whereas indirect interactions seem to favor jettison of effector genes.
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              Innate immunity in plants: an arms race between pattern recognition receptors in plants and effectors in microbial pathogens.

              For many years, research on a suite of plant defense responses that begin when plants are exposed to general microbial elicitors was underappreciated, for a good reason: There has been no critical experimental demonstration of their importance in mediating plant resistance during pathogen infection. Today, these microbial elicitors are named pathogen- or microbe-associated molecular patterns (PAMPs or MAMPs) and the plant responses are known as PAMP-triggered immunity (PTI). Recent studies provide an elegant explanation for the difficulty of demonstrating the role of PTI in plant disease resistance. It turns out that the important contribution of PTI to disease resistance is masked by pathogen virulence effectors that have evolved to suppress it.
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                Author and article information

                Journal
                Open Biol
                Open Biol
                RSOB
                royopenbio
                Open Biology
                The Royal Society
                2046-2441
                May 2017
                3 May 2017
                3 May 2017
                : 7
                : 5
                : 170057
                Affiliations
                State Key Laboratory of Wheat and Maize Crop Science/Collaborative Innovation Center of Henan Grain Crops, College of Life Science, Henan Agricultural University , Zhengzhou 450002, People's Republic of China
                Author notes
                [†]

                These authors contributed equally to this study.

                Author information
                http://orcid.org/0000-0002-7709-2164
                Article
                rsob170057
                10.1098/rsob.170057
                5451545
                28469008
                c49ca6a6-97af-45cf-80f6-970a1c0f3392
                © 2017 The Authors.

                Published by the Royal Society under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/4.0/, which permits unrestricted use, provided the original author and source are credited.

                History
                : 6 March 2017
                : 5 April 2017
                Funding
                Funded by: Plan for scientific innovation talent of henan province;
                Award ID: 154200510024
                Funded by: Key Project of Henan Province;
                Award ID: 161100110400
                Funded by: the national key basic research program of china;
                Award ID: 2013CB127702
                Categories
                1001
                129
                200
                199
                Review
                Review Article
                Custom metadata
                May 2017

                Life sciences
                fungal pathogens,host plant,early infection,molecular interactions,avirulent genes,resistance genes

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