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Gregory B Martin - One of the best experts on this subject based on the ideXlab platform.
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wrky22 and wrky25 transcription factors are positive regulators of defense responses in nicotiana benthamiana
Plant Molecular Biology, 2021Co-Authors: Romina Nair Ramos, Marina A. Pombo, Gregory B Martin, Hernan G RosliAbstract:NbWRKY22 and NbWRKY25 are required for full activation of bacteria-associated pattern- and Effector-Triggered Immunity as well as for the response to other non-bacterial defense elicitors. Plants defend themselves against pathogens using a two-layered immune system. Pattern-triggered Immunity (PTI) can be activated upon recognition of epitopes from flagellin including flg22. Pseudomonas syringae pv. tomato (Pst) delivers effector proteins into the plant cell to promote host susceptibility. However, some plants express resistance (R) proteins that recognize specific effectors leading to the activation of Effector-Triggered Immunity (ETI). Resistant tomato lines such as Rio Grande-PtoR (RG-PtoR) recognize two Pst effectors, AvrPto and AvrPtoB, and activate ETI through the Pto/Prf protein complex. Using RNA-seq, we identified two tomato WRKY transcription factor genes, SlWRKY22 and SlWRKY25, whose expression is increased during Pst-induced ETI. Silencing of the WRKY25/22 orthologous genes in Nicotiana benthamiana led to a delay in programmed cell death normally associated with AvrPto recognition or several non-bacterial effector/R protein pairs. An increase in disease symptoms was observed in silenced plants infiltrated with Pseudomonas syringae pv. tabaci expressing AvrPto or HopQ1-1. Expression of both tomato WRKY genes is also induced upon treatment with flg22 and callose deposition and cell death suppression assays in WRKY25/22-silenced N. benthamiana plants supported their involvement in PTI. Our results reveal an important role for two WRKYs as positive regulators of plant Immunity against bacterial and potentially non-bacterial pathogens.
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WRKY22 and WRKY25 transcription factors are positive regulators of defense responses in Nicotiana benthamiana
Plant Molecular Biology, 2020Co-Authors: Romina Nair Ramos, Marina A. Pombo, Gregory B Martin, Hernan G RosliAbstract:Key message NbWRKY22 and NbWRKY25 are required for full activation of bacteria-associated pattern- and Effector-Triggered Immunity as well as for the response to other non-bacterial defense elicitors. Abstract Plants defend themselves against pathogens using a two-layered immune system. Pattern-triggered Immunity (PTI) can be activated upon recognition of epitopes from flagellin including flg22. Pseudomonas syringae pv. tomato ( Pst ) delivers effector proteins into the plant cell to promote host susceptibility. However, some plants express resistance (R) proteins that recognize specific effectors leading to the activation of Effector-Triggered Immunity (ETI). Resistant tomato lines such as Rio Grande-PtoR (RG-PtoR) recognize two Pst effectors, AvrPto and AvrPtoB, and activate ETI through the Pto/Prf protein complex. Using RNA-seq, we identified two tomato WRKY transcription factor genes, SlWRKY22 and SlWRKY25 , whose expression is increased during Pst -induced ETI. Silencing of the WRKY25/22 orthologous genes in Nicotiana benthamiana led to a delay in programmed cell death normally associated with AvrPto recognition or several non-bacterial effector/R protein pairs. An increase in disease symptoms was observed in silenced plants infiltrated with Pseudomonas syringae pv . tabaci expressing AvrPto or HopQ1-1. Expression of both tomato WRKY genes is also induced upon treatment with flg22 and callose deposition and cell death suppression assays in WRKY25/22- silenced N. benthamiana plants supported their involvement in PTI. Our results reveal an important role for two WRKYs as positive regulators of plant Immunity against bacterial and potentially non-bacterial pathogens.
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transcriptomic analysis reveals tomato genes whose expression is induced specifically during effector triggered Immunity and identifies the epk1 protein kinase which is required for the host response to three bacterial effector proteins
Genome Biology, 2014Co-Authors: Marina A. Pombo, Diane M. Dunham, Zhangjun Fei, Gregory B Martin, Yi Zheng, Noe FernandezpozoAbstract:Background: Plants have two related immune systems to defend themselves against pathogen attack. Initially, pattern-triggered Immunity is activated upon recognition of microbe-associated molecular patterns by pattern recognition receptors. Pathogenic bacteria deliver effector proteins into the plant cell that interfere with this immune response and promote disease. However, some plants express resistance proteins that detect the presence of specific effectors leading to a robust defense response referred to as Effector-Triggered Immunity. The interaction of tomato with Pseudomonas syringae pv. tomato is an established model system for understanding the molecular basis of these plant immune responses. Results: We apply high-throughput RNA sequencing to this pathosystem to identify genes whose expression changes specifically during pattern-triggered or Effector-Triggered Immunity. We then develop reporter genes for each of these responses that will enable characterization of the host response to the large collection of P. s. pv. tomato strains that express different combinations of effectors. Virus-induced gene silencing of 30 of the Effector-Triggered Immunity-specific genes identifies Epk1 which encodes a predicted protein kinase from a family previously unknown to be involved in Immunity. Knocked-down expression of Epk1 compromises Effector-Triggered Immunity triggered by three bacterial effectors but not by effectors from non-bacterial pathogens. Epistasis experiments indicate that Epk1 acts upstream of Effector-Triggered Immunity-associated MAP kinase signaling.
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Transcriptomic analysis reveals tomato genes whose expression is induced specifically during Effector-Triggered Immunity and identifies the Epk1 protein kinase which is required for the host response to three bacterial effector proteins
Genome biology, 2014Co-Authors: Marina A. Pombo, Noe Fernandez-pozo, Diane M. Dunham, Zhangjun Fei, Yi Zheng, Gregory B MartinAbstract:BACKGROUND: Plants have two related immune systems to defend themselves against pathogen attack. Initially,pattern-triggered Immunity is activated upon recognition of microbe-associated molecular patterns by pattern recognition receptors. Pathogenic bacteria deliver effector proteins into the plant cell that interfere with this immune response and promote disease. However, some plants express resistance proteins that detect the presence of specific effectors leading to a robust defense response referred to as Effector-Triggered Immunity. The interaction of tomato with Pseudomonas syringae pv. tomato is an established model system for understanding the molecular basis of these plant immune responses.\n\nRESULTS: We apply high-throughput RNA sequencing to this pathosystem to identify genes whose expression changes specifically during pattern-triggered or Effector-Triggered Immunity. We then develop reporter genes for each of these responses that will enable characterization of the host response to the large collection of P. s. pv. tomato strains that express different combinations of effectors. Virus-induced gene silencing of 30 of the Effector-Triggered Immunity-specific genes identifies Epk1 which encodes a predicted protein kinase from a family previously unknown to be involved in Immunity. Knocked-down expression of Epk1 compromises Effector-Triggered Immunity triggered by three bacterial effectors but not by effectors from non-bacterial pathogens. Epistasis experiments indicate that Epk1 acts upstream of Effector-Triggered Immunity-associated MAP kinase signaling.\n\nCONCLUSIONS: Using RNA-seq technology we identify genes involved in specific immune responses. A functional genomics screen led to the discovery of Epk1, a novel predicted protein kinase required for plant defense activation upon recognition of three different bacterial effectors.
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Effector-Triggered Immunity mediated by the Pto kinase.
Trends in plant science, 2010Co-Authors: Gregory B MartinAbstract:Pto was the first disease-resistance gene cloned from a plant that confers recognition of a specific pathogen. The intracellular protein kinase that it encodes activates an immune response in tomato (Solanum lycopersicum) to bacterial speck disease by interacting with either the AvrPto or AvrPtoB type III effector proteins that are delivered into the plant cell by Pseudomonas syringae pathovar tomato. This recognition event triggers signaling pathways leading to Effector-Triggered Immunity (ETI), which inhibits pathogen growth. During the past 15 years, ∼25 genes have been identified by loss-of-function studies to have a role in Pto-mediated ETI. Here, we review the experimental approaches that have been used in these studies, discuss the proteins that have been identified and characterized, and present a current model of Pto-mediated ETI.
Darrell Desveaux - One of the best experts on this subject based on the ideXlab platform.
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The Arabidopsis ZED1-Related Kinase Genomic Cluster Is Specifically Required for Effector-Triggered Immunity.
Plant physiology, 2020Co-Authors: Derek Seto, Bradley Laflamme, David S Guttman, Darrell DesveauxAbstract:CRISPR / Cas9 - mediated deletion of an Arabidopsis gene cluster encoding eight kinases supports their Immunity - specific roles in sensing pathogenic effectors .
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the pan genome effector triggered Immunity landscape of a host pathogen interaction
Science, 2020Co-Authors: Bradley Laflamme, Marcus M Dillon, Alexandre Martel, Renan N D Almeida, Darrell Desveaux, David S GuttmanAbstract:Effector-Triggered Immunity (ETI), induced by host immune receptors in response to microbial effectors, protects plants against virulent pathogens. However, a systematic study of ETI prevalence against species-wide pathogen diversity is lacking. We constructed the Pseudomonas syringae Type III Effector Compendium (PsyTEC) to reduce the pan-genome complexity of 5127 unique effector proteins, distributed among 70 families from 494 strains, to 529 representative alleles. We screened PsyTEC on the model plant Arabidopsis thaliana and identified 59 ETI-eliciting alleles (11.2%) from 19 families (27.1%), with orthologs distributed among 96.8% of P. syringae strains. We also identified two previously undescribed host immune receptors, including CAR1, which recognizes the conserved effectors AvrE and HopAA1, and found that 94.7% of strains harbor alleles predicted to be recognized by either CAR1 or ZAR1.
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Elevated Temperature Differentially Influences Effector-Triggered Immunity Outputs in Arabidopsis.
Frontiers in plant science, 2015Co-Authors: Alexandra Menna, David S Guttman, Dang Nguyen, Darrell DesveauxAbstract:Pseudomonas syringae is a Gram-negative bacterium that infects multiple plant species by manipulating cellular processes via injection of type three secreted effectors (T3SEs) into host cells. Nucleotide-binding leucine-rich repeat (NLR) resistance (R) proteins recognize specific T3SEs and trigger a robust immune response, called Effector-Triggered Immunity (ETI), which limits pathogen proliferation and is often associated with localized programmed cell death, known as the hypersensitive response (HR). In this study, we examine the influence of elevated temperature on two ETI outputs: HR and pathogen virulence suppression. We found that in the Arabidopsis thaliana accession Col-0, elevated temperatures suppress the HR, but have minimal influence on ETI-associated P. syringae virulence suppression, thereby uncoupling these two ETI responses. We also identify accessions of Arabidopsis that exhibit impaired P. syringae virulence suppression at elevated temperature, highlighting the natural variation that exists in coping with biotic and abiotic stresses. These results not only reinforce the influence of abiotic factors on plant Immunity but also emphasize the importance of carefully documented environmental conditions in studies of plant Immunity.
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Proteomics of Effector-Triggered Immunity (ETI) in plants
Virulence, 2014Co-Authors: Brenden A. Hurley, David S Guttman, Rajagopal Subramaniam, Darrell DesveauxAbstract:Effector-Triggered Immunity (ETI) was originally termed gene-for-gene resistance and dates back to fundamental observations of flax resistance to rust fungi by Harold Henry Flor in the 1940s. Since then, genetic and biochemical approaches have defined our current understanding of how plant “resistance” proteins recognize microbial effectors. More recently, proteomic approaches have expanded our view of the protein landscape during ETI and contributed significant advances to our mechanistic understanding of ETI signaling. Here we provide an overview of proteomic techniques that have been used to study plant ETI including both global and targeted approaches. We discuss the challenges associated with ETI proteomics and highlight specific examples from the literature, which demonstrate how proteomics is advancing the ETI research field.
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The rise of the undead: Pseudokinases as mediators of Effector-Triggered Immunity
Plant signaling & behavior, 2014Co-Authors: Jennifer D. Lewis, David S Guttman, Patrick Bastedo, Darrell DesveauxAbstract:Pathogens use effector proteins to suppress host Immunity and promote infection. However, plants can recognize specific effectors and mount an Effector-Triggered immune response that suppresses pathogen growth. The YopJ/HopZ family of type III secreted effector proteins is broadly distributed in bacterial pathogens of both animals and plants. These effectors can either suppress host Immunity or elicit defense responses depending on the host genotype. In a recent report, we identified an Arabidopsis thaliana pseudokinase ZED1 that is required for the recognition of the Pseudomonas syringae HopZ1a effector. Here we discuss the role of ZED1 in HopZ1a recognition, and present models of effector recognition in plants. We draw parallels between HopZ1a and YopJ effector proteins, and between ZED1 and other Immunity-related kinases that can be targeted by pathogen effectors.
Marina A. Pombo - One of the best experts on this subject based on the ideXlab platform.
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wrky22 and wrky25 transcription factors are positive regulators of defense responses in nicotiana benthamiana
Plant Molecular Biology, 2021Co-Authors: Romina Nair Ramos, Marina A. Pombo, Gregory B Martin, Hernan G RosliAbstract:NbWRKY22 and NbWRKY25 are required for full activation of bacteria-associated pattern- and Effector-Triggered Immunity as well as for the response to other non-bacterial defense elicitors. Plants defend themselves against pathogens using a two-layered immune system. Pattern-triggered Immunity (PTI) can be activated upon recognition of epitopes from flagellin including flg22. Pseudomonas syringae pv. tomato (Pst) delivers effector proteins into the plant cell to promote host susceptibility. However, some plants express resistance (R) proteins that recognize specific effectors leading to the activation of Effector-Triggered Immunity (ETI). Resistant tomato lines such as Rio Grande-PtoR (RG-PtoR) recognize two Pst effectors, AvrPto and AvrPtoB, and activate ETI through the Pto/Prf protein complex. Using RNA-seq, we identified two tomato WRKY transcription factor genes, SlWRKY22 and SlWRKY25, whose expression is increased during Pst-induced ETI. Silencing of the WRKY25/22 orthologous genes in Nicotiana benthamiana led to a delay in programmed cell death normally associated with AvrPto recognition or several non-bacterial effector/R protein pairs. An increase in disease symptoms was observed in silenced plants infiltrated with Pseudomonas syringae pv. tabaci expressing AvrPto or HopQ1-1. Expression of both tomato WRKY genes is also induced upon treatment with flg22 and callose deposition and cell death suppression assays in WRKY25/22-silenced N. benthamiana plants supported their involvement in PTI. Our results reveal an important role for two WRKYs as positive regulators of plant Immunity against bacterial and potentially non-bacterial pathogens.
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WRKY22 and WRKY25 transcription factors are positive regulators of defense responses in Nicotiana benthamiana
Plant Molecular Biology, 2020Co-Authors: Romina Nair Ramos, Marina A. Pombo, Gregory B Martin, Hernan G RosliAbstract:Key message NbWRKY22 and NbWRKY25 are required for full activation of bacteria-associated pattern- and Effector-Triggered Immunity as well as for the response to other non-bacterial defense elicitors. Abstract Plants defend themselves against pathogens using a two-layered immune system. Pattern-triggered Immunity (PTI) can be activated upon recognition of epitopes from flagellin including flg22. Pseudomonas syringae pv. tomato ( Pst ) delivers effector proteins into the plant cell to promote host susceptibility. However, some plants express resistance (R) proteins that recognize specific effectors leading to the activation of Effector-Triggered Immunity (ETI). Resistant tomato lines such as Rio Grande-PtoR (RG-PtoR) recognize two Pst effectors, AvrPto and AvrPtoB, and activate ETI through the Pto/Prf protein complex. Using RNA-seq, we identified two tomato WRKY transcription factor genes, SlWRKY22 and SlWRKY25 , whose expression is increased during Pst -induced ETI. Silencing of the WRKY25/22 orthologous genes in Nicotiana benthamiana led to a delay in programmed cell death normally associated with AvrPto recognition or several non-bacterial effector/R protein pairs. An increase in disease symptoms was observed in silenced plants infiltrated with Pseudomonas syringae pv . tabaci expressing AvrPto or HopQ1-1. Expression of both tomato WRKY genes is also induced upon treatment with flg22 and callose deposition and cell death suppression assays in WRKY25/22- silenced N. benthamiana plants supported their involvement in PTI. Our results reveal an important role for two WRKYs as positive regulators of plant Immunity against bacterial and potentially non-bacterial pathogens.
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transcriptomic analysis reveals tomato genes whose expression is induced specifically during effector triggered Immunity and identifies the epk1 protein kinase which is required for the host response to three bacterial effector proteins
Genome Biology, 2014Co-Authors: Marina A. Pombo, Diane M. Dunham, Zhangjun Fei, Gregory B Martin, Yi Zheng, Noe FernandezpozoAbstract:Background: Plants have two related immune systems to defend themselves against pathogen attack. Initially, pattern-triggered Immunity is activated upon recognition of microbe-associated molecular patterns by pattern recognition receptors. Pathogenic bacteria deliver effector proteins into the plant cell that interfere with this immune response and promote disease. However, some plants express resistance proteins that detect the presence of specific effectors leading to a robust defense response referred to as Effector-Triggered Immunity. The interaction of tomato with Pseudomonas syringae pv. tomato is an established model system for understanding the molecular basis of these plant immune responses. Results: We apply high-throughput RNA sequencing to this pathosystem to identify genes whose expression changes specifically during pattern-triggered or Effector-Triggered Immunity. We then develop reporter genes for each of these responses that will enable characterization of the host response to the large collection of P. s. pv. tomato strains that express different combinations of effectors. Virus-induced gene silencing of 30 of the Effector-Triggered Immunity-specific genes identifies Epk1 which encodes a predicted protein kinase from a family previously unknown to be involved in Immunity. Knocked-down expression of Epk1 compromises Effector-Triggered Immunity triggered by three bacterial effectors but not by effectors from non-bacterial pathogens. Epistasis experiments indicate that Epk1 acts upstream of Effector-Triggered Immunity-associated MAP kinase signaling.
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Transcriptomic analysis reveals tomato genes whose expression is induced specifically during Effector-Triggered Immunity and identifies the Epk1 protein kinase which is required for the host response to three bacterial effector proteins
Genome biology, 2014Co-Authors: Marina A. Pombo, Noe Fernandez-pozo, Diane M. Dunham, Zhangjun Fei, Yi Zheng, Gregory B MartinAbstract:BACKGROUND: Plants have two related immune systems to defend themselves against pathogen attack. Initially,pattern-triggered Immunity is activated upon recognition of microbe-associated molecular patterns by pattern recognition receptors. Pathogenic bacteria deliver effector proteins into the plant cell that interfere with this immune response and promote disease. However, some plants express resistance proteins that detect the presence of specific effectors leading to a robust defense response referred to as Effector-Triggered Immunity. The interaction of tomato with Pseudomonas syringae pv. tomato is an established model system for understanding the molecular basis of these plant immune responses.\n\nRESULTS: We apply high-throughput RNA sequencing to this pathosystem to identify genes whose expression changes specifically during pattern-triggered or Effector-Triggered Immunity. We then develop reporter genes for each of these responses that will enable characterization of the host response to the large collection of P. s. pv. tomato strains that express different combinations of effectors. Virus-induced gene silencing of 30 of the Effector-Triggered Immunity-specific genes identifies Epk1 which encodes a predicted protein kinase from a family previously unknown to be involved in Immunity. Knocked-down expression of Epk1 compromises Effector-Triggered Immunity triggered by three bacterial effectors but not by effectors from non-bacterial pathogens. Epistasis experiments indicate that Epk1 acts upstream of Effector-Triggered Immunity-associated MAP kinase signaling.\n\nCONCLUSIONS: Using RNA-seq technology we identify genes involved in specific immune responses. A functional genomics screen led to the discovery of Epk1, a novel predicted protein kinase required for plant defense activation upon recognition of three different bacterial effectors.
Walter Gassmann - One of the best experts on this subject based on the ideXlab platform.
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The Arabidopsis immune adaptor SRFR1 interacts with TCP transcription factors that redundantly contribute to Effector-Triggered Immunity.
The Plant journal : for cell and molecular biology, 2014Co-Authors: Sang Hee Kim, Saikat Bhattacharjee, Geon Hui Son, Hye Jin Kim, Ji Chul Nam, Phuong Dung T. Nguyen, Jong Chan Hong, Walter GassmannAbstract:Summary The plant immune system must be tightly controlled both positively and negatively to maintain normal plant growth and health. We previously identified SUPPRESSOR OF rps4-RLD1 (SRFR1) as a negative regulator specifically of Effector-Triggered Immunity. SRFR1 is localized in both a cytoplasmic microsomal compartment and in the nucleus. Its TPR domain has sequence similarity to TPR domains of transcriptional repressors in other organisms, suggesting that SRFR1 may negatively regulate Effector-Triggered Immunity via transcriptional control. We show here that excluding SRFR1 from the nucleus prevented complementation of the srfr1 phenotype. To identify transcription factors that interact with SRFR1, we screened an Arabidopsis transcription factor prey library by yeast two-hybrid assay and isolated six class I members of the TEOSINTE BRANCHED1/CYCLOIDEA/PCF (TCP) transcription factor family. Specific interactions were verified in planta. Although single or double T-DNA mutant tcp8, tcp14 or tcp15 lines were not more susceptible to bacteria expressing AvrRps4, the triple tcp8 tcp14 tcp15 mutant displayed decreased Effector-Triggered Immunity mediated by the resistance genes RPS2, RPS4, RPS6 and RPM1. In addition, expression of PATHOGENESIS-RELATED PROTEIN2 was attenuated in srfr1-4 tcp8-1 tcp14-5 tcp15-3 plants compared to srfr1-4 plants. To date, TCP transcription factors have been implicated mostly in developmental processes. Our data indicate that one function of a subset of TCP proteins is to regulate defense gene expression in antagonism to SRFR1, and suggest a mechanism for an intimate connection between plant development and Immunity.
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New clues in the nucleus: transcriptional reprogramming in Effector-Triggered Immunity.
Frontiers in plant science, 2013Co-Authors: Saikat Bhattacharjee, Christopher M. Garner, Walter GassmannAbstract:The robustness of plant Effector-Triggered Immunity is correlated with massive alterations of the host transcriptome. Yet the molecular mechanisms that cause and underlie this reprogramming remain obscure. Here we will review recent advances in deciphering nuclear functions of plant immune receptors and of associated proteins. Important open questions remain, such as the identities of the primary transcription factors involved in control of Effector-Triggered immune responses, and indeed whether this can be generalized or whether particular effector-resistance protein interactions impinge on distinct sectors in the transcriptional response web. Multiple lines of evidence have implicated WRKY transcription factors at the core of responses to microbe-associated molecular patterns and in intersections with Effector-Triggered Immunity. Recent findings from yeast two-hybrid studies suggest that members of the TCP transcription factor family are targets of several effectors from diverse pathogens. Additional transcription factor families that are directly or indirectly involved in Effector-Triggered Immunity are likely to be identified.
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Effector-Triggered Immunity signaling: from gene-for-gene pathways to protein-protein interaction networks.
Molecular plant-microbe interactions : MPMI, 2012Co-Authors: Walter Gassmann, Saikat BhattacharjeeAbstract:In its simplicity and testability, Flor's gene-for-gene hypothesis has been a powerful driver in plant Immunity research for decades. Once the molecular underpinnings of gene-for-gene resistance had come into sharper focus, there was a reassessment of Flor's hypothesis and a name change to Effector-Triggered Immunity. As implied by the name change and exemplified by pioneering studies, plant Immunity is increasingly described in terms of protein rather than genetic interactions. This progress leads to a reinterpretation of old concepts of pathogen recognition and resistance signaling and, of course, opens up new questions. Here, we provide a brief historical overview of resistance gene function and how a new focus on protein interactions can lead to a deeper understanding of the logic of plant innate Immunity signaling.
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Pathogen effectors target Arabidopsis EDS1 and alter its interactions with immune regulators.
Science (New York N.Y.), 2011Co-Authors: Saikat Bhattacharjee, Sang Hee Kim, Morgan K. Halane, Walter GassmannAbstract:Plant resistance proteins detect the presence of specific pathogen effectors and initiate Effector-Triggered Immunity. Few immune regulators downstream of resistance proteins have been identified, none of which are known virulence targets of effectors. We show that Arabidopsis ENHANCED DISEASE SUSCEPTIBILITY1 (EDS1), a positive regulator of basal resistance and of Effector-Triggered Immunity specifically mediated by Toll–interleukin-1 receptor–nucleotide binding–leucine-rich repeat (TIR-NB-LRR) resistance proteins, forms protein complexes with the TIR-NB-LRR disease resistance proteins RPS4 and RPS6 and with the negative immune regulator SRFR1 at a cytoplasmic membrane. Further, the cognate bacterial effectors AvrRps4 and HopA1 disrupt these EDS1 complexes. Tight association of EDS1 with TIR-NB-LRR–mediated Immunity may therefore derive mainly from being guarded by TIR-NB-LRR proteins, and activation of this branch of Effector-Triggered Immunity may directly connect to the basal resistance signaling pathway via EDS1.
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SRFR1, a suppressor of Effector-Triggered Immunity, encodes a conserved tetratricopeptide repeat protein with similarity to transcriptional repressors.
The Plant journal : for cell and molecular biology, 2008Co-Authors: Soon Il Kwon, Saikat Bhattacharjee, Sang Hee Kim, Jae-jong Noh, Walter GassmannAbstract:Summary Effector-Triggered Immunity provides plants with strong protection from pathogens. However, this response has the potential to be highly deleterious to the host and needs to be tightly controlled. The molecular mechanisms in the plant that regulate the balance between activation and suppression of resistance are not fully understood. Previously, we identified Arabidopsis suppressor of rps4-RLD 1 (srfr1) mutants with enhanced resistance to the bacterial effector AvrRps4. These mutants were recessive and retained full susceptibility to virulent bacteria, suggesting that SRFR1 functions as a negative regulator and that AvrRps4-triggered Immunity was specifically enhanced in the mutants. Consistent with this, we show here that the response to flagellin, an elicitor of basal resistance, is unaltered in srfr1-1. In contrast, resistance to AvrRps4 in srfr1-1 requires EDS1, a central regulator of Effector-Triggered Immunity via multiple resistance genes. SRFR1 is a single-copy gene encoding a pioneer tetratricopeptide repeat protein conserved between plants and animals. The SRFR1 tetratricopeptide repeat domain shows sequence similarity to those of transcriptional repressors in Saccharomyces cerevisiae and Caenorhabditis elegans. Indeed, a sub-pool of SRFR1 transiently expressed in Nicotiana benthamiana leaf cells localizes to the nucleus. Identification of SRFR1 may therefore provide insight into the regulation of the transcriptional reprogramming that is activated by Effector-Triggered Immunity.
Saikat Bhattacharjee - One of the best experts on this subject based on the ideXlab platform.
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The Arabidopsis immune adaptor SRFR1 interacts with TCP transcription factors that redundantly contribute to Effector-Triggered Immunity.
The Plant journal : for cell and molecular biology, 2014Co-Authors: Sang Hee Kim, Saikat Bhattacharjee, Geon Hui Son, Hye Jin Kim, Ji Chul Nam, Phuong Dung T. Nguyen, Jong Chan Hong, Walter GassmannAbstract:Summary The plant immune system must be tightly controlled both positively and negatively to maintain normal plant growth and health. We previously identified SUPPRESSOR OF rps4-RLD1 (SRFR1) as a negative regulator specifically of Effector-Triggered Immunity. SRFR1 is localized in both a cytoplasmic microsomal compartment and in the nucleus. Its TPR domain has sequence similarity to TPR domains of transcriptional repressors in other organisms, suggesting that SRFR1 may negatively regulate Effector-Triggered Immunity via transcriptional control. We show here that excluding SRFR1 from the nucleus prevented complementation of the srfr1 phenotype. To identify transcription factors that interact with SRFR1, we screened an Arabidopsis transcription factor prey library by yeast two-hybrid assay and isolated six class I members of the TEOSINTE BRANCHED1/CYCLOIDEA/PCF (TCP) transcription factor family. Specific interactions were verified in planta. Although single or double T-DNA mutant tcp8, tcp14 or tcp15 lines were not more susceptible to bacteria expressing AvrRps4, the triple tcp8 tcp14 tcp15 mutant displayed decreased Effector-Triggered Immunity mediated by the resistance genes RPS2, RPS4, RPS6 and RPM1. In addition, expression of PATHOGENESIS-RELATED PROTEIN2 was attenuated in srfr1-4 tcp8-1 tcp14-5 tcp15-3 plants compared to srfr1-4 plants. To date, TCP transcription factors have been implicated mostly in developmental processes. Our data indicate that one function of a subset of TCP proteins is to regulate defense gene expression in antagonism to SRFR1, and suggest a mechanism for an intimate connection between plant development and Immunity.
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New clues in the nucleus: transcriptional reprogramming in Effector-Triggered Immunity.
Frontiers in plant science, 2013Co-Authors: Saikat Bhattacharjee, Christopher M. Garner, Walter GassmannAbstract:The robustness of plant Effector-Triggered Immunity is correlated with massive alterations of the host transcriptome. Yet the molecular mechanisms that cause and underlie this reprogramming remain obscure. Here we will review recent advances in deciphering nuclear functions of plant immune receptors and of associated proteins. Important open questions remain, such as the identities of the primary transcription factors involved in control of Effector-Triggered immune responses, and indeed whether this can be generalized or whether particular effector-resistance protein interactions impinge on distinct sectors in the transcriptional response web. Multiple lines of evidence have implicated WRKY transcription factors at the core of responses to microbe-associated molecular patterns and in intersections with Effector-Triggered Immunity. Recent findings from yeast two-hybrid studies suggest that members of the TCP transcription factor family are targets of several effectors from diverse pathogens. Additional transcription factor families that are directly or indirectly involved in Effector-Triggered Immunity are likely to be identified.
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Effector-Triggered Immunity signaling: from gene-for-gene pathways to protein-protein interaction networks.
Molecular plant-microbe interactions : MPMI, 2012Co-Authors: Walter Gassmann, Saikat BhattacharjeeAbstract:In its simplicity and testability, Flor's gene-for-gene hypothesis has been a powerful driver in plant Immunity research for decades. Once the molecular underpinnings of gene-for-gene resistance had come into sharper focus, there was a reassessment of Flor's hypothesis and a name change to Effector-Triggered Immunity. As implied by the name change and exemplified by pioneering studies, plant Immunity is increasingly described in terms of protein rather than genetic interactions. This progress leads to a reinterpretation of old concepts of pathogen recognition and resistance signaling and, of course, opens up new questions. Here, we provide a brief historical overview of resistance gene function and how a new focus on protein interactions can lead to a deeper understanding of the logic of plant innate Immunity signaling.
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Pathogen effectors target Arabidopsis EDS1 and alter its interactions with immune regulators.
Science (New York N.Y.), 2011Co-Authors: Saikat Bhattacharjee, Sang Hee Kim, Morgan K. Halane, Walter GassmannAbstract:Plant resistance proteins detect the presence of specific pathogen effectors and initiate Effector-Triggered Immunity. Few immune regulators downstream of resistance proteins have been identified, none of which are known virulence targets of effectors. We show that Arabidopsis ENHANCED DISEASE SUSCEPTIBILITY1 (EDS1), a positive regulator of basal resistance and of Effector-Triggered Immunity specifically mediated by Toll–interleukin-1 receptor–nucleotide binding–leucine-rich repeat (TIR-NB-LRR) resistance proteins, forms protein complexes with the TIR-NB-LRR disease resistance proteins RPS4 and RPS6 and with the negative immune regulator SRFR1 at a cytoplasmic membrane. Further, the cognate bacterial effectors AvrRps4 and HopA1 disrupt these EDS1 complexes. Tight association of EDS1 with TIR-NB-LRR–mediated Immunity may therefore derive mainly from being guarded by TIR-NB-LRR proteins, and activation of this branch of Effector-Triggered Immunity may directly connect to the basal resistance signaling pathway via EDS1.
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SRFR1, a suppressor of Effector-Triggered Immunity, encodes a conserved tetratricopeptide repeat protein with similarity to transcriptional repressors.
The Plant journal : for cell and molecular biology, 2008Co-Authors: Soon Il Kwon, Saikat Bhattacharjee, Sang Hee Kim, Jae-jong Noh, Walter GassmannAbstract:Summary Effector-Triggered Immunity provides plants with strong protection from pathogens. However, this response has the potential to be highly deleterious to the host and needs to be tightly controlled. The molecular mechanisms in the plant that regulate the balance between activation and suppression of resistance are not fully understood. Previously, we identified Arabidopsis suppressor of rps4-RLD 1 (srfr1) mutants with enhanced resistance to the bacterial effector AvrRps4. These mutants were recessive and retained full susceptibility to virulent bacteria, suggesting that SRFR1 functions as a negative regulator and that AvrRps4-triggered Immunity was specifically enhanced in the mutants. Consistent with this, we show here that the response to flagellin, an elicitor of basal resistance, is unaltered in srfr1-1. In contrast, resistance to AvrRps4 in srfr1-1 requires EDS1, a central regulator of Effector-Triggered Immunity via multiple resistance genes. SRFR1 is a single-copy gene encoding a pioneer tetratricopeptide repeat protein conserved between plants and animals. The SRFR1 tetratricopeptide repeat domain shows sequence similarity to those of transcriptional repressors in Saccharomyces cerevisiae and Caenorhabditis elegans. Indeed, a sub-pool of SRFR1 transiently expressed in Nicotiana benthamiana leaf cells localizes to the nucleus. Identification of SRFR1 may therefore provide insight into the regulation of the transcriptional reprogramming that is activated by Effector-Triggered Immunity.
