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      Disease Resistance Mechanisms in Plants

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          Abstract

          Plants have developed a complex defense system against diverse pests and pathogens. Once pathogens overcome mechanical barriers to infection, plant receptors initiate signaling pathways driving the expression of defense response genes. Plant immune systems rely on their ability to recognize enemy molecules, carry out signal transduction, and respond defensively through pathways involving many genes and their products. Pathogens actively attempt to evade and interfere with response pathways, selecting for a decentralized, multicomponent immune system. Recent advances in molecular techniques have greatly expanded our understanding of plant immunity, largely driven by potential application to agricultural systems. Here, we review the major plant immune system components, state of the art knowledge, and future direction of research on plant–pathogen interactions. In our review, we will discuss how the decentralization of plant immune systems have provided both increased evolutionary opportunity for pathogen resistance, as well as additional mechanisms for pathogen inhibition of such defense responses. We conclude that the rapid advances in bioinformatics and molecular biology are driving an explosion of information that will advance agricultural production and illustrate how complex molecular interactions evolve.

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          Most cited references276

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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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            Perception of the bacterial PAMP EF-Tu by the receptor EFR restricts Agrobacterium-mediated transformation.

            Higher eukaryotes sense microbes through the perception of pathogen-associated molecular patterns (PAMPs). Arabidopsis plants detect a variety of PAMPs including conserved domains of bacterial flagellin and of bacterial EF-Tu. Here, we show that flagellin and EF-Tu activate a common set of signaling events and defense responses but without clear synergistic effects. Treatment with either PAMP results in increased binding sites for both PAMPs. We used this finding in a targeted reverse-genetic approach to identify a receptor kinase essential for EF-Tu perception, which we called EFR. Nicotiana benthamiana, a plant unable to perceive EF-Tu, acquires EF-Tu binding sites and responsiveness upon transient expression of EFR. Arabidopsis efr mutants show enhanced susceptibility to the bacterium Agrobacterium tumefaciens, as revealed by a higher efficiency of T-DNA transformation. These results demonstrate that EFR is the EF-Tu receptor and that plant defense responses induced by PAMPs such as EF-Tu reduce transformation by Agrobacterium.
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              A flagellin-induced complex of the receptor FLS2 and BAK1 initiates plant defence.

              Plants sense potential microbial invaders by using pattern-recognition receptors to recognize pathogen-associated molecular patterns (PAMPs). In Arabidopsis thaliana, the leucine-rich repeat receptor kinases flagellin-sensitive 2 (FLS2) (ref. 2) and elongation factor Tu receptor (EFR) (ref. 3) act as pattern-recognition receptors for the bacterial PAMPs flagellin and elongation factor Tu (EF-Tu) (ref. 5) and contribute to resistance against bacterial pathogens. Little is known about the molecular mechanisms that link receptor activation to intracellular signal transduction. Here we show that BAK1 (BRI1-associated receptor kinase 1), a leucine-rich repeat receptor-like kinase that has been reported to regulate the brassinosteroid receptor BRI1 (refs 6,7), is involved in signalling by FLS2 and EFR. Plants carrying bak1 mutations show normal flagellin binding but abnormal early and late flagellin-triggered responses, indicating that BAK1 acts as a positive regulator in signalling. The bak1-mutant plants also show a reduction in early, but not late, EF-Tu-triggered responses. The decrease in responses to PAMPs is not due to reduced sensitivity to brassinosteroids. We provide evidence that FLS2 and BAK1 form a complex in vivo, in a specific ligand-dependent manner, within the first minutes of stimulation with flagellin. Thus, BAK1 is not only associated with developmental regulation through the plant hormone receptor BRI1 (refs 6,7), but also has a functional role in PRR-dependent signalling, which initiates innate immunity.
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                Author and article information

                Journal
                Genes (Basel)
                Genes (Basel)
                genes
                Genes
                MDPI
                2073-4425
                04 July 2018
                July 2018
                : 9
                : 7
                : 339
                Affiliations
                [1 ]Department of Biology and Microbiology, South Dakota State University, Brookings, 57007 SD, USA; ethan.andersen@ 123456sdstate.edu (E.A.); yang.yen@ 123456sdstate.edu (Y.Y.)
                [2 ]Department of Agronomy, Horticulture, and Plant Science, South Dakota State University, Brookings, 57007 SD, USA; shaukat.ali@ 123456sdstate.edu (S.A.); emmanuel.byamukama@ 123456sdstate.edu (E.B.)
                Author notes
                [* ]Correspondence: madhav.nepal@ 123456sdstate.edu ; Tel.: +1-605-688-5971
                Author information
                https://orcid.org/0000-0002-1055-8636
                https://orcid.org/0000-0001-5565-523X
                Article
                genes-09-00339
                10.3390/genes9070339
                6071103
                29973557
                84849561-e621-4a06-911a-e93a383ad705
                © 2018 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 31 May 2018
                : 29 June 2018
                Categories
                Review

                coevolution,defense response,disease resistance,nucleotide-binding leucine-rich repeat,plant immunity,plant-pest interaction,pathogenesis,pattern recognition receptor,phytopathology,resistance gene

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