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      Different Pathogen Defense Strategies in Arabidopsis: More than Pathogen Recognition

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          Abstract

          Plants constantly suffer from simultaneous infection by multiple pathogens, which can be divided into biotrophic, hemibiotrophic, and necrotrophic pathogens, according to their lifestyles. Many studies have contributed to improving our knowledge of how plants can defend against pathogens, involving different layers of defense mechanisms. In this sense, the review discusses: (1) the functions of PAMP (pathogen-associated molecular pattern)-triggered immunity (PTI) and effector-triggered immunity (ETI), (2) evidence highlighting the functions of salicylic acid (SA) and jasmonic acid (JA)/ethylene (ET)-mediated signaling pathways downstream of PTI and ETI, and (3) other defense aspects, including many novel small molecules that are involved in defense and phenomena, including systemic acquired resistance (SAR) and priming. In particular, we mainly focus on SA and (JA)/ET-mediated signaling pathways. Interactions among them, including synergistic effects and antagonistic effects, are intensively explored. This might be critical to understanding dynamic disease regulation.

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

          Cyril Zipfel, Gernot Kunze, Delphine Chinchilla … (2006)
          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.

            Delphine Chinchilla, Cyril Zipfel, Silke Robatzek … (2007)
            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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              Fungal small RNAs suppress plant immunity by hijacking host RNA interference pathways.

              Arne Weiberg, Ming Wang, Feng-Mao Lin … (2013)
              Botrytis cinerea, the causative agent of gray mold disease, is an aggressive fungal pathogen that infects more than 200 plant species. Here, we show that some B. cinerea small RNAs (Bc-sRNAs) can silence Arabidopsis and tomato genes involved in immunity. These Bc-sRNAs hijack the host RNA interference (RNAi) machinery by binding to Arabidopsis Argonaute 1 (AGO1) and selectively silencing host immunity genes. The Arabidopsis ago1 mutant exhibits reduced susceptibility to B. cinerea, and the B. cinerea dcl1 dcl2 double mutant that can no longer produce these Bc-sRNAs displays reduced pathogenicity on Arabidopsis and tomato. Thus, this fungal pathogen transfers "virulent" sRNA effectors into host plant cells to suppress host immunity and achieve infection, which demonstrates a naturally occurring cross-kingdom RNAi as an advanced virulence mechanism.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Cells
                Journal ID (iso-abbrev): Cells
                Journal ID (publisher-id): cells
                Title: Cells
                Publisher: MDPI
                ISSN (Electronic): 2073-4409
                Publication date (Electronic): 07 December 2018
                Publication date Collection: December 2018
                Volume: 7
                Issue: 12
                Electronic Location Identifier: 252
                Affiliations
                [1 ]College of Bioengineering, Sichuan University of Science and Engineering, Zigong 643000, China; zhangwei19840117@ 123456163.com (W.Z.); jianglihui19940625@ 123456163.com (L.J.)
                [2 ]Helmholtz Zentrum München, Department of Environmental Sciences, Institute of Biochemical Plant Pathology, Ingolstädter Landstr. 1, 85764 Neuherberg, Germany; feng.zhao@ 123456helmholtz-muenchen.de
                [3 ]College of Chemistry and Life Science, Chengdu Normal University, Chengdu 611130, China; chencun0211@ 123456126.com
                [4 ]West Rape Research Institute, Guizhou Academy of Agricultural Sciences, Guizhou 550008, China; wult12@ 123456126.com
                [5 ]Key Laboratory of Bio-Resources and Eco-Environment of Ministry of Education, College of Life Sciences, Sichuan University, Chengdu 610064, China
                Author notes
                [* ]Correspondence: liuzhibin@ 123456scu.edu.cn ; Tel.: +86-028-8541-2281
                Article
                Publisher ID: cells-07-00252
                DOI: 10.3390/cells7120252
                PMC ID: 6315839
                PubMed ID: 30544557
                SO-VID: a7374840-0b09-4bfc-b26f-9626394e2622
                Copyright © © 2018 by the authors.
                License:

                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
                Date received : 19 October 2018
                Date accepted : 03 December 2018
                Categories
                Subject: Review

                Keywords: pathogen defense,pti,eti,hormone pathways,small molecules,sar,priming
                Data availability:
                Keywords: pathogen defense, pti, eti, hormone pathways, small molecules, sar, priming

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