scholarly journals Recognitional Specificity and Evolution in the Tomato–Cladosporium fulvum Pathosystem

2009 ◽  
Vol 22 (10) ◽  
pp. 1191-1202 ◽  
Author(s):  
B. B. H. Wulff ◽  
A. Chakrabarti ◽  
D. A. Jones
Keyword(s):  
Defense Mechanisms ◽  
Extracellular Proteins ◽  
Effector Proteins ◽  
Cladosporium Fulvum ◽  
Host Proteins ◽  
Pathogen Effectors ◽  
Passalora Fulva ◽  
Pathogen Effector ◽  
Mold Fungus ◽  
Avr Genes

The interactions between plants and many biotrophic or hemibiotrophic pathogens are controlled by receptor proteins in the host and effector proteins delivered by the pathogen. Pathogen effectors facilitate pathogen growth through the suppression of host defenses and the manipulation of host metabolism, but recognition of a pathogen-effector protein by a host receptor enables the host to activate a suite of defense mechanisms that limit pathogen growth. In the tomato (Lycopersicon esculentum syn. Solanum lycopersicum)–Cladosporium fulvum (leaf mold fungus syn. Passalora fulva) pathosystem, the host receptors are plasma membrane–anchored, leucine-rich repeat, receptor-like proteins encoded by an array of Cf genes conferring resistance to C. fulvum. The pathogen effectors are mostly small, secreted, cysteine-rich, but otherwise largely dissimilar, extracellular proteins encoded by an array of avirulence (Avr) genes, so called because of their ability to trigger resistance and limit pathogen growth when the corresponding Cf gene is present in tomato. A number of Cf and Avr genes have been isolated, and details of the complex molecular interplay between tomato Cf proteins and C. fulvum effector proteins are beginning to emerge. Each effector appears to have a different role; probably most bind or modify different host proteins, but at least one has a passive role masking the pathogen. It is, therefore, not surprising that each effector is probably detected in a distinct and specific manner, some by direct binding, others as complexes with host proteins, and others via their modification of host proteins. The two papers accompanying this review contribute further to our understanding of the molecular specificity underlying effector perception by Cf proteins. This review, therefore, focuses on our current understanding of recognitional specificity in the tomato–C. fulvum pathosystem and highlights some of the critical questions that remain to be addressed. It also addresses the evolutionary causes and consequences of this specificity.

scholarly journals The blast pathogen effector AVR-Pik binds and stabilizes rice heavy metal-associated (HMA) proteins to co-opt their function in immunity

2020 ◽  
Author(s):  
K. Oikawa ◽  
K. Fujisaki ◽  
M. Shimizu ◽  
T. Takeda ◽  
H. Saitoh ◽  
...  
Keyword(s):  
Heavy Metal ◽  
Susceptibility Gene ◽  
Leucine Rich Repeat ◽  
Nucleotide Binding Domain ◽  
Host Proteins ◽  
Immune Receptors ◽  
Pathogen Effectors ◽  
Pathogen Effector ◽  
Integrated Domains ◽  
Complex Architecture

AbstractPlant intracellular nucleotide-binding domain and leucine-rich repeat-containing (NLR) immune receptors have a complex architecture. They can include noncanonical integrated domains that are thought to have evolved from host targets of pathogen effectors to serve as pathogen baits. However, the functions of host proteins with similarity to NLR integrated domains and the extent to which they are targeted by pathogen effectors remain largely unknown. Here, we show that the blast fungus effector AVR-Pik binds a subset of related rice proteins containing a heavy metal-associated (HMA) domain, one of the domains that has repeatedly integrated into plant NLR immune receptors. We find that AVR-Pik binding stabilizes the rice HMA proteins OsHIPP19 and OsHIPP20. Knockout of OsHIPP20 causes enhanced disease resistance towards the blast pathogen, indicating that OsHIPP20 is a susceptibility gene (S-gene). We propose that AVR-Pik has evolved to bind HMA domain proteins and co-opt their function to suppress immunity. Yet this binding carries a trade-off, it triggers immunity in plants carrying NLR receptors with integrated HMA domains.

scholarly journals Sustained Incompatibility between MAPK Signaling and Pathogen Effectors

2020 ◽  
Vol 21 (21) ◽  
pp. 7954
Author(s):  
Julien Lang ◽  
Jean Colcombet
Keyword(s):  
Defense Responses ◽  
Mapk Signaling ◽  
Effector Proteins ◽  
Plant Defense Responses ◽  
Pathogen Effectors ◽  
Current State ◽  
Pathogen Effector ◽  
Mitogen Activated Protein ◽  
Effector Triggered Immunity ◽  
Signaling Components

In plants, Mitogen-Activated Protein Kinases (MAPKs) are important signaling components involved in developemental processes as well as in responses to biotic and abiotic stresses. In this review, we focus on the roles of MAPKs in Effector-Triggered Immunity (ETI), a specific layer of plant defense responses dependent on the recognition of pathogen effector proteins. Having inspected the literature, we synthesize the current state of knowledge concerning this topic. First, we describe how pathogen effectors can manipulate MAPK signaling to promote virulence, and how in parallel plants have developed mechanisms to protect themselves against these interferences. Then, we discuss the striking finding that the recognition of pathogen effectors can provoke a sustained activation of the MAPKs MPK3/6, extensively analyzing its implications in terms of regulation and functions. In line with this, we also address the question of how a durable activation of MAPKs might affect the scope of their substrates, and thereby mediate the emergence of possibly new ETI-specific responses. By highlighting the sometimes conflicting or missing data, our intention is to spur further research in order to both consolidate and expand our understanding of MAPK signaling in immunity.

scholarly journals A Survey on Occurrence of Cladosporium fulvum Identifies Race 0 and Race 2 in Tomato-Growing Areas of Argentina

Plant Disease ◽  
2015 ◽  
Vol 99 (12) ◽  
pp. 1732-1737 ◽  
Author(s):  
Rocío Medina ◽  
Silvina M. Y. López ◽  
Mario E. E. Franco ◽  
Cristina Rollan ◽  
Blanca L. Ronco ◽  
...  
Keyword(s):  
Leaf Tissue ◽  
Morphological Characters ◽  
Cladosporium Fulvum ◽  
Greenhouse Production ◽  
Passalora Fulva ◽  
Race Identity ◽  
Race 2 ◽  
Production Areas ◽  
Avr Genes

The presence of Cladosporium fulvum (syn. Passalora fulva), causal agent of tomato leaf mold, was confirmed in the two main greenhouse-production areas for tomato in Argentina. Using both morphological characters and internal transcribed spacer sequencing, we confirmed the presence of physiological races of this pathogen. A diagnostic multiplex polymerase chain reaction (PCR) was also developed, using primers derived from C. fulvum avirulence (Avr) genes. In all, 20 isolates of Cladosporium spp. were obtained as monospore cultures and 12 were identified as C. fulvum. By this method, we showed that, of these 12 isolates, 5 were race 0 (carrying functional Avr2, Avr4, Avr4E, and Avr9 genes) and 7 were race 2 (lacking the Avr2 gene). Race identity was confirmed by testing their virulence on a set of tomato differentials carrying different Cf resistance genes. All Avr genes could be amplified in single or multiplex PCR using DNA isolated from in vitro grown monospore cultures but only three Avr could be amplified when genomic DNA was isolated from C. fulvum-infected necrotic leaf tissue.

scholarly journals An unconventional NOI/RIN4 domain of a rice NLR protein binds host EXO70 protein to confer fungal immunity

2017 ◽  
Author(s):  
Koki Fujisaki ◽  
Yoshiko Abe ◽  
Eiko Kanzaki ◽  
Kazue Ito ◽  
Hiroe Utsushi ◽  
...  
Keyword(s):  
Host Protein ◽  
Current View ◽  
Nucleotide Binding Domain ◽  
Host Proteins ◽  
Core Motif ◽  
Pathogen Effectors ◽  
Pathogen Effector ◽  
Integrated Domains ◽  
Effector Recognition ◽  
Fungal Immunity

A subset of plant nucleotide-binding domain and leucine-rich repeat-containing (NLR) proteins carry extraneous integrated domains that have been proposed to mediate pathogen effector recognition. The current view is that these unconventional domains function by directly binding or serving as substrates for pathogen effectors, yet only a few domains have been functionally characterized to date. Here we report that the integrated NOI domain of the rice NLR protein Pii-2, together with its partner Pii-1, mediates immunity to the rice blast fungus Magnaporthe oryzae by indirect recognition of the AVR-Pii effector. We discovered that the Pii-2 NOI domain does not physically interact with the effector itself but instead binds the host protein OsExo70-F3, which is a target of AVR-Pii. We further identified mutations within the NOI core motif (PxFGxW) of Pii-2 that abolish both OsExo70-F3 binding and Pii-mediated resistance to M. oryzae expressing AVR-Pii. This led us to propose a novel conceptual model in which an NLR-integrated domain functions to detect host proteins targeted by pathogen effectors, in a framework that extends classical indirect recognition models.

scholarly journals Harnessing Effector-Triggered Immunity for Durable Disease Resistance

2017 ◽  
Vol 107 (8) ◽  
pp. 912-919 ◽  
Author(s):  
Meixiang Zhang ◽  
Gitta Coaker
Keyword(s):  
Disease Resistance ◽  
Plant Pathogens ◽  
Domain Architecture ◽  
Effector Proteins ◽  
Plant Diseases ◽  
Sources Of Resistance ◽  
Pathogen Effectors ◽  
Pathogen Effector ◽  
Effector Triggered Immunity ◽  
Durable Disease Resistance

Genetic control of plant diseases has traditionally included the deployment of single immune receptors with nucleotide-binding leucine-rich repeat (NLR) domain architecture. These NLRs recognize corresponding pathogen effector proteins inside plant cells, resulting in effector-triggered immunity (ETI). Although ETI triggers robust resistance, deployment of single NLRs can be rapidly overcome by pathogen populations within a single or a few growing seasons. In order to generate more durable disease resistance against devastating plant pathogens, a multitiered strategy that incorporates stacked NLRs combined with other sources of disease resistance is necessary. New genetic and genomic technologies have enabled advancements in identifying conserved pathogen effectors, isolating NLR repertoires from diverse plants, and editing plant genomes to enhance resistance. Significant advancements have also been made in understanding plant immune perception at the receptor level, which has promise for engineering new sources of resistance. Here, we discuss how to utilize recent scientific advancements in a multilayered strategy for developing more durable disease resistance.

scholarly journals Pathogen effector recognition-dependent association of NRG1 with EDS1 and SAG101 in TNL receptor immunity

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Xinhua Sun ◽  
Dmitry Lapin ◽  
Joanna M. Feehan ◽  
Sara C. Stolze ◽  
Katharina Kramer ◽  
...  
Keyword(s):  
Disease Susceptibility ◽  
Nucleotide Binding ◽  
Molecular Evidence ◽  
Pathogen Effectors ◽  
Pathogen Effector ◽  
Family Protein ◽  
Activated State ◽  
Defence Signalling ◽  
Effector Recognition ◽  
Dependent Interaction

AbstractPlants utilise intracellular nucleotide-binding, leucine-rich repeat (NLR) immune receptors to detect pathogen effectors and activate local and systemic defence. NRG1 and ADR1 “helper” NLRs (RNLs) cooperate with enhanced disease susceptibility 1 (EDS1), senescence-associated gene 101 (SAG101) and phytoalexin-deficient 4 (PAD4) lipase-like proteins to mediate signalling from TIR domain NLR receptors (TNLs). The mechanism of RNL/EDS1 family protein cooperation is not understood. Here, we present genetic and molecular evidence for exclusive EDS1/SAG101/NRG1 and EDS1/PAD4/ADR1 co-functions in TNL immunity. Using immunoprecipitation and mass spectrometry, we show effector recognition-dependent interaction of NRG1 with EDS1 and SAG101, but not PAD4. An EDS1-SAG101 complex interacts with NRG1, and EDS1-PAD4 with ADR1, in an immune-activated state. NRG1 requires an intact nucleotide-binding P-loop motif, and EDS1 a functional EP domain and its partner SAG101, for induced association and immunity. Thus, two distinct modules (NRG1/EDS1/SAG101 and ADR1/EDS1/PAD4) mediate TNL receptor defence signalling.

scholarly journals Agroinfiltration for transient gene expression and characterisation of fungal pathogen effectors in cool-season grain legume hosts

2021 ◽  
Author(s):  
Johannes W. Debler ◽  
Bernadette M. Henares ◽  
Robert C. Lee
Keyword(s):  
Broad Spectrum ◽  
Faba Bean ◽  
Fluorescent Protein ◽  
Transient Gene Expression ◽  
Low Frequency ◽  
Effector Proteins ◽  
Field Pea ◽  
Grain Legume ◽  
Pathogen Effectors ◽  
Green Fluorescent

Abstract Key message Modified pEAQ-HT-DEST1 vectors were used for agroinfiltration in legumes. We demonstrate protein expression and export in pea, lentil, and faba bean; however, the method for chickpea was not successful. Abstract Agroinfiltration is a valuable research method for investigating virulence and avirulence effector proteins from pathogens and pests, where heterologous effector proteins are transiently expressed in plant leaves and hypersensitive necrosis responses and other effector functions can be assessed. Nicotiana benthamiana is widely used for agroinfiltration and the characterisation of broad-spectrum effectors. The method has also been used in other plant species including field pea, but not yet developed for chickpea, lentil, or faba bean. Here, we have modified the pEAQ-HT-DEST1 vector for expression of 6 × histidine-tagged green-fluorescent protein (GFP) and the known necrosis-inducing broad-spectrum effector necrosis and ethylene-inducing peptide (Nep1)-like protein (NLP). Modified pEAQ-based vectors were adapted to encode signal peptide sequences for apoplast targeting of expressed proteins. We used confocal microscopy to assess the level of GFP expression in agroinfiltrated leaves. While at 3 days after infiltration in N. benthamiana, GFP was expressed at a relatively high level, expression in field pea and faba bean at the same time point was relatively low. In lentil, an expression level of GFP similar to field pea and faba bean at 3 days was only observed after 5 days. Chickpea leaf cells were transformed at low frequency and agroinfiltration was concluded to not be successful for chickpea. We concluded that the pEAQ vector is suitable for testing host-specific effectors in field pea, lentil, and faba bean, but low transformation efficiency limits the utility of the method for chickpea.

scholarly journals Molecular Basis of Citrus sunki Susceptibility and Poncirus trifoliata Resistance Upon Phytophthora parasitica Attack

2018 ◽  
Vol 31 (3) ◽  
pp. 386-398 ◽  
Author(s):  
Ronaldo José Durigan Dalio ◽  
Heros José Máximo ◽  
Tiago Silva Oliveira ◽  
Thamara de Medeiros Azevedo ◽  
Henrique Leme Felizatti ◽  
...  
Keyword(s):  
Molecular Basis ◽  
Defense Mechanisms ◽  
Time Course ◽  
Poncirus Trifoliata ◽  
Disease Development ◽  
Phytophthora Parasitica ◽  
Defense Strategies ◽  
Molecular Core ◽  
Pathogen Effector ◽  
Plant Pathogen Interactions

Coevolution has shaped the molecular basis of an extensive number of defense mechanisms in plant-pathogen interactions. Phytophthora parasitica, a hemibiothrophic oomycete pathogen and the causal agent of citrus root rot and gummosis, interacts differently with Citrus sunki and Poncirus trifoliata, two commonly favored citrus rootstocks that are recognized as susceptible and resistant, respectively, to P. parasitica. The molecular core of these interactions remains elusive. Here, we provide evidence on the defense strategies employed by both susceptible and resistant citrus rootstocks, in parallel with P. parasitica deployment of effectors. Time course expression analysis (quantitative real-time polymerase chain reaction) of several defense-related genes were evaluated during i) plant disease development, ii) necrosis, and iii) pathogen effector gene expression. In C. sunki, P. parasitica deploys effectors, including elicitins, NPP1 (necrosis-inducing Phytophthora protein 1), CBEL (cellulose-binding elicitor and lectin activity), RxLR, and CRN (crinkler), and, consequently, this susceptible plant activates its main defense signaling pathways that result in the hypersensitive response and necrosis. Despite the strong plant-defense response, it fails to withstand P. parasitica invasion, confirming its hemibiothrophic lifestyle. In Poncirus trifoliata, the effectors were strongly expressed, nevertheless failing to induce any immunity manipulation and disease development, suggesting a nonhost resistance type, in which the plant relies on preformed biochemical and anatomical barriers.

scholarly journals Affinity-tags are removed from Cladosporium fulvum effector proteins expressed in the tomato leaf apoplast

2006 ◽  
Vol 57 (3) ◽  
pp. 599-608 ◽  
Author(s):  
H. Peter van Esse ◽  
Bart P. H. J. Thomma ◽  
John W. van 't Klooster ◽  
Pierre J. G. M. de Wit
Keyword(s):  
Tomato Leaf ◽  
Effector Proteins ◽  
Cladosporium Fulvum ◽  
Affinity Tags ◽  
Leaf Apoplast

scholarly journals Cooperative Immune Suppression by Escherichia coli and Shigella Effector Proteins

2018 ◽  
Vol 86 (4) ◽  
Author(s):  
Maarten F. de Jong ◽  
Neal M. Alto
Keyword(s):  
Escherichia Coli ◽  
Defense Mechanisms ◽  
Immune Defense ◽  
Effector Proteins ◽  
Innate Immune ◽  
Host Cells ◽  
Secretion Systems ◽  
Content Type ◽  
E Coli ◽  
Type Iii Secretion Systems

ABSTRACT The enteric attaching and effacing (A/E) pathogens enterohemorrhagic Escherichia coli (EHEC) and enteropathogenic E. coli (EPEC) and the invasive pathogens enteroinvasive E. coli (EIEC) and Shigella encode type III secretion systems (T3SS) used to inject effector proteins into human host cells during infection. Among these are a group of effectors required for NF-κB-mediated host immune evasion. Recent studies have identified several effector proteins from A/E pathogens and EIEC/ Shigella that are involved in suppression of NF-κB and have uncovered their cellular and molecular functions. A novel mechanism among these effectors from both groups of pathogens is to coordinate effector function during infection. This cooperativity among effector proteins explains how bacterial pathogens are able to effectively suppress innate immune defense mechanisms in response to diverse classes of immune receptor signaling complexes (RSCs) stimulated during infection.

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