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Nature Communications: Plant immune response to pathogens differs with changing temperatures

Nature Communications: Plant immune response to pathogens differs with changing temperatures | Effectors | Scoop.it
ABSTRACT: Temperature fluctuation is a key determinant for microbial invasion and host evasion. In contrast to mammals that maintain constant body temperature, plant temperature oscillates on a daily basis. It remains elusive how plants operate inducible defenses in response to temperature fluctuation. Here we report that ambient temperature changes lead to pronounced shifts of the following two distinct plant immune responses: pattern-triggered immunity (PTI) and effector-triggered immunity (ETI). Plants preferentially activate ETI signaling at relatively low temperatures (10–23 °C), whereas they switch to PTI signaling at moderately elevated temperatures (23–32 °C). The Arabidopsis arp6 and hta9hta11 mutants, phenocopying plants grown at elevated temperatures, exhibit enhanced PTI and yet reduced ETI responses. As the secretion of bacterial effectors favours low temperatures, whereas bacteria multiply vigorously at elevated temperatures accompanied with increased microbe-associated molecular pattern production, our findings suggest that temperature oscillation might have driven dynamic co-evolution of distinct plant immune signaling responding to pathogen physiological changes.
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Nature Communication - Plant immune response to pathogens differs with changing temperatures

Abstract: Temperature fluctuation is a key determinant for microbial invasion and host evasion. In contrast to mammals that maintain constant body temperature, plant temperature oscillates on a daily basis. It remains elusive how plants operate inducible defenses in response to temperature fluctuation. Here we report that ambient temperature changes lead to pronounced shifts of the following two distinct plant immune responses: pattern-triggered immunity (PTI) and effector-triggered immunity (ETI). Plants preferentially activate ETI signaling at relatively low temperatures (10–23 °C), whereas they switch to PTI signaling at moderately elevated temperatures (23–32 °C). The Arabidopsis arp6 andhta9hta11 mutants, phenocopying plants grown at elevated temperatures, exhibit enhanced PTI and yet reduced ETI responses. As the secretion of bacterial effectors favours low temperatures, whereas bacteria multiply vigorously at elevated temperatures accompanied with increased microbe-associated molecular pattern production, our findings suggest that temperature oscillation might have driven dynamic co-evolution of distinct plant immune signaling responding to pathogen physiological changes.
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Intrinsic Disorder in Pathogen Effectors: Protein Flexibility as an Evolutionary Hallmark in a Molecular Arms Race

Intrinsic Disorder in Pathogen Effectors: Protein Flexibility as an Evolutionary Hallmark in a Molecular Arms Race | Effectors | Scoop.it
Effector proteins represent a refined mechanism of bacterial pathogens to overcome plants’ innate immune systems. These modular proteins often manipulate host physiology by directly interfering with immune signaling of plant cells. Even if host cells have developed efficient strategies to perceive the presence of pathogenic microbes and to recognize intracellular effector activity, it remains an open question why only few effectors are recognized directly by plant resistance proteins. Based on in-silico genome-wide surveys and a reevaluation of published structural data, we estimated that bacterial effectors of phytopathogens are highly enriched in long-disordered regions (>50 residues). These structurally flexible segments have no secondary structure under physiological conditions but can fold in a stimulus-dependent manner (e.g., during protein–protein interactions). The high abundance of intrinsic disorder in effectors strongly suggests positive evolutionary selection of this structural feature and highlights the dynamic nature of these proteins. We postulate that such structural flexibility may be essential for (1) effector translocation, (2) evasion of the innate immune system, and (3) host function mimicry. The study of these dynamical regions will greatly complement current structural approaches to understand the molecular mechanisms of these proteins and may help in the prediction of new effectors.
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PLOS Pathogens: A Pathogen Type III Effector with a Novel E3 Ubiquitin Ligase Architecture (2013)

PLOS Pathogens: A Pathogen Type III Effector with a Novel E3 Ubiquitin Ligase Architecture (2013) | Effectors | Scoop.it
Type III effectors are virulence factors of Gram-negative bacterial pathogens delivered directly into host cells by the type III secretion nanomachine where they manipulate host cell processes such as the innate immunity and gene expression. Here, we show that the novel type III effector XopL from the model plant pathogen Xanthomonas campestris pv. vesicatoriaexhibits E3 ubiquitin ligase activity in vitro and in planta, induces plant cell death and subverts plant immunity. E3 ligase activity is associated with the C-terminal region of XopL, which specifically interacts with plant E2 ubiquitin conjugating enzymes and mediates formation of predominantly K11-linked polyubiquitin chains. The crystal structure of the XopL C-terminal domain revealed a single domain with a novel fold, termed XL-box, not present in any previously characterized E3 ligase. Mutation of amino acids in the central cavity of the XL-box disrupts E3 ligase activity and prevents XopL-induced plant cell death. The lack of cysteine residues in the XL-box suggests the absence of thioester-linked ubiquitin-E3 ligase intermediates and a non-catalytic mechanism for XopL-mediated ubiquitination. The crystal structure of the N-terminal region of XopL confirmed the presence of a leucine-rich repeat (LRR) domain, which may serve as a protein-protein interaction module for ubiquitination target recognition. While the E3 ligase activity is required to provoke plant cell death, suppression of PAMP responses solely depends on the N-terminal LRR domain. Taken together, the unique structural fold of the E3 ubiquitin ligase domain within the Xanthomonas XopL is unprecedented and highlights the variation in bacterial pathogen effectors mimicking this eukaryote-specific activity.
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Recognition of bacterial plant pathogens: local, systemic and transgenerational immunity - Henry - 2013 - New Phytologist - Wiley Online Library

Recognition of bacterial plant pathogens: local, systemic and transgenerational immunity - Henry - 2013 - New Phytologist - Wiley Online Library | Effectors | Scoop.it
Bacterial pathogens can cause multiple plant diseases and plants rely on their innate immune system to recognize and actively respond to these microbes. The plant innate immune system comprises extracellular pattern recognition receptors that recognize conserved microbial patterns and intracellular nucleotide binding leucine-rich repeat (NLR) proteins that recognize specific bacterial effectors delivered into host cells. Plants lack the adaptive immune branch present in animals, but still afford flexibility to pathogen attack through systemic and transgenerational resistance. Here, we focus on current research in plant immune responses against bacterial pathogens. Recent studies shed light onto the activation and inactivation of pattern recognition receptors and systemic acquired resistance. New research has also uncovered additional layers of complexity surrounding NLR immune receptor activation, cooperation and sub-cellular localizations. Taken together, these recent advances bring us closer to understanding the web of molecular interactions responsible for coordinating defense responses and ultimately resistance.
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Pseudomonas syringae pv. tomato DC3000: A Model Pathogen for Probing Disease Susceptibility and Hormone Signaling in Plants

Pseudomonas syringae pv. tomato DC3000: A Model Pathogen for Probing Disease Susceptibility and Hormone Signaling in Plants | Effectors | Scoop.it
Scooped from: Annual Review of Phytopathology, 2013 Authors: Xiu-Fang Xin and Sheng Yang He Summary: Since the early 1980s, various strains of the gram-negative bacterial pathogen Pseudomonas syringae have been used as models for understanding plant-bacterial interactions. In 1991, a P. syringae pathovar tomato (Pst) strain, DC3000, was reported to infect not only its natural host tomato but also Arabidopsis in the laboratory, a finding that spurred intensive efforts in the subsequent two decades to characterize the molecular mechanisms by which this strain causes disease in plants. Genomic analysis shows that Pst DC3000 carries a large repertoire of potential virulence factors, including proteinaceous effectors that are secreted through the type III secretion system and a polyketide phytotoxin called coronatine, which structurally mimics the plant hormone jasmonate ( JA). Study of Pst DC3000 pathogenesis has not only provided several conceptual advances in understanding how a bacterial pathogen employs type III effectors to suppress plant immune responses and promote disease susceptibility but has also facilitated the discovery of the immune function of stomata and key components of JA signaling in plants. The concepts derived from the study of Pst DC3000 pathogenesis may prove useful in understanding pathogenesis mechanisms of other plant pathogens.
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Pathogen blocks host death receptor signalling by arginine GlcNAcylation of ... - Nature.com

Pathogen blocks host death receptor signalling by arginine GlcNAcylation of ... Nature.com NleB probably functions as part of a network of effectors during EPEC interaction with the host.
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PLOS Pathogens: The Salmonella Type III Effector SspH2 Specifically Exploits the NLR Co-chaperone Activity of SGT1 to Subvert Immunity (2013)

PLOS Pathogens: The Salmonella Type III Effector SspH2 Specifically Exploits the NLR Co-chaperone Activity of SGT1 to Subvert Immunity (2013) | Effectors | Scoop.it
To further its pathogenesis, S. Typhimurium delivers effector proteins into host cells, including the novel E3 ubiquitin ligase (NEL) effector SspH2. Using model systems in a cross-kingdom approach we gained further insight into the molecular function of this effector. Here, we show that SspH2 modulates innate immunity in both mammalian and plant cells. In mammalian cell culture, SspH2 significantly enhanced Nod1-mediated IL-8 secretion when transiently expressed or bacterially delivered. In addition, SspH2 also enhanced an Rx-dependent hypersensitive response in planta. In both of these nucleotide-binding leucine rich repeat receptor (NLR) model systems, SspH2-mediated phenotypes required its catalytic E3 ubiquitin ligase activity and interaction with the conserved host protein SGT1. SGT1 has an essential cell cycle function and an additional function as an NLR co-chaperone in animal and plant cells. Interaction between SspH2 and SGT1 was restricted to SGT1 proteins that have NLR co-chaperone function and accordingly, SspH2 did not affect SGT1 cell cycle functions. Mechanistic studies revealed that SspH2 interacted with, and ubiquitinated Nod1 and could induce Nod1 activity in an agonist-independent manner if catalytically active. Interestingly, SspH2 in vitro ubiquitination activity and protein stability were enhanced by SGT1. Overall, this work adds to our understanding of the sophisticated mechanisms used by bacterial effectors to co-opt host pathways by demonstrating that SspH2 can subvert immune responses by selectively exploiting the functions of a conserved host co-chaperone.
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Plant Cell: Intrinsic Disorder in Pathogen Effectors: Protein Flexibility as an Evolutionary Hallmark in a Molecular Arms Race (2013)

Plant Cell: Intrinsic Disorder in Pathogen Effectors: Protein Flexibility as an Evolutionary Hallmark in a Molecular Arms Race (2013) | Effectors | Scoop.it
Effector proteins represent a refined mechanism of bacterial pathogens to overcome plants’ innate immune systems. These modular proteins often manipulate host physiology by directly interfering with immune signaling of plant cells. Even if host cells have developed efficient strategies to perceive the presence of pathogenic microbes and to recognize intracellular effector activity, it remains an open question why only few effectors are recognized directly by plant resistance proteins. Based on in-silico genome-wide surveys and a reevaluation of published structural data, we estimated that bacterial effectors of phytopathogens are highly enriched in long-disordered regions (>50 residues). These structurally flexible segments have no secondary structure under physiological conditions but can fold in a stimulus-dependent manner (e.g., during protein–protein interactions). The high abundance of intrinsic disorder in effectors strongly suggests positive evolutionary selection of this structural feature and highlights the dynamic nature of these proteins. We postulate that such structural flexibility may be essential for (1) effector translocation, (2) evasion of the innate immune system, and (3) host function mimicry. The study of these dynamical regions will greatly complement current structural approaches to understand the molecular mechanisms of these proteins and may help in the prediction of new effectors.
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New Phytologist: Five phylogenetically close rice SWEET genes confer TAL effector-mediated susceptibility to Xanthomonas oryzae pv. oryzae (2013)

New Phytologist: Five phylogenetically close rice SWEET genes confer TAL effector-mediated susceptibility to Xanthomonas oryzae pv. oryzae (2013) | Effectors | Scoop.it
Bacterial plant-pathogenic Xanthomonas strains translocate transcription activator-like (TAL) effectors into plant cells to function as specific transcription factors. Only a few plant target genes of TAL effectors have been identified, so far. Three plant SWEET genes encoding putative sugar transporters are known to be induced by TAL effectors from rice-pathogenic Xanthomonas oryzae pv. oryzae (Xoo). We predict and validate that expression of OsSWEET14 is induced by a novel TAL effector, Tal5, from an African Xoo strain. Artificial TAL effectors (ArtTALs) were constructed to individually target 20 SWEET orthologs in rice. They were used as designer virulence factors to study which rice SWEET genes can support Xoo virulence. The Tal5 target box differs from those of the already known TAL effectors TalC, AvrXa7 and PthXo3, which also induce expression of OsSWEET14, suggesting evolutionary convergence on key targets. ArtTALs efficiently complemented an Xoo talC mutant, demonstrating that specific induction of OsSWEET14 is the key target of TalC. ArtTALs that specifically target individual members of the rice SWEET family revealed three known and two novel SWEET genes to support bacterial virulence. Our results demonstrate that five phylogenetically close SWEET proteins, which presumably act as sucrose transporters, can support Xoo virulence.
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Actin Cytoskeleton Manipulation by Effector Proteins Secreted by ...

Actin Cytoskeleton Manipulation by Effector Proteins Secreted by ... | Effectors | Scoop.it
An interesting model to study actin manipulation by bacterial effectors is Escherichia coli since due to its genome plasticity it has acquired diverse genetic mobile elements, which allow having different E.
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Nature Reviews Immunology: Effector-triggered versus pattern-triggered immunity: how animals sense pathogens (2013)

Nature Reviews Immunology: Effector-triggered versus pattern-triggered immunity: how animals sense pathogens (2013) | Effectors | Scoop.it
http://www.nature.com/nri/journal/vaop/ncurrent/full/nri3398.html A fundamental question regarding any immune system is how it can discriminate between pathogens and non-pathogens. Here, we discuss how this discrimination can be mediated by a surveillance system distinct from pattern-recognition receptors that recognize conserved microbial patterns. It can be based instead on the ability of the host to sense perturbations in host cells induced by bacterial toxins or 'effectors' that are encoded by pathogenic microorganisms. Such 'effector-triggered immunity' was previously demonstrated mainly in plants, but recent data confirm that animals can also use this strategy.
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Secretome analysis of the rice bacterium Xanthomonas oryzae (Xoo) using in vitro and in planta systems

Secretome analysis of the rice bacterium Xanthomonas oryzae (Xoo) using in vitro and in planta systems | Effectors | Scoop.it
Summary: Xanthomonas oryzae pv. oryzae (Xoo) causes bacterial blight disease in rice, and that severely affects yield loss (upto 50%) of total rice production. Here, we report a proteomics investigation of Xoo (compatible race K3)-secreted proteins, isolated from its in vitro culture and in planta infected rice leaves. Two-dimensional gel electrophoresis (2-DE) coupled with MALDI-TOF-MS and/or nLC-ESI-MS/MS approach identified 139 protein spots (out of 153 differential spots), encoding 109 unique proteins. Identified proteins belonged to multiple biological and molecular functions. Metabolic and nutrient uptake proteins were common up to both in vitro and in planta secretomes. However, pathogenicity, protease/peptidase, and host defense-related proteins were highly- or specifically-expressed during in planta infection. A good correlation was observed between protein and transcript abundances for nine proteins-secreted in planta as per semi-quantitative RT-PCR analysis. Transgenic rice leaf sheath (carrying PBZ1 promoter::GFP cell death reporter), when used to express a few of the identified secretory proteins, showed a direct activation of cell death signaling, suggesting their involvement in pathogenicity-related with secretion effectors. This work furthers our understanding of rice bacterial blight disease, and serves as a resource for possible translation in generating disease resistant rice plants for improved seed yield.
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A novel effector secretion mechanism based on proton-motive force-dependent type III secretion apparatus rotation

A novel effector secretion mechanism based on proton-motive force-dependent type III secretion apparatus rotation | Effectors | Scoop.it
Scooped from: The Journal of the Federation of American Societies for Experimental Biology, 2013 Authors: Takashi Ohgita, Naoki Hayashi, Susumu Hama, Hiroyuki Tsuchiya, Naomasa Gotoh and Kentaro Kogure Summary: The type III secretion apparatus (T3SA) participates in the secretion of bacterial proteins called effectors, although the detailed mechanism of effector secretion remains unclear. T3SA and flagellum were shown to branch from a common ancestor and also show structural similarity. In addition, both T3SA-dependent effector secretion and flagellar rotation were reported to require proton-motive force (PMF) for activity. From these reports, we hypothesized that T3SA, like the flagellum, would rotate via PMF and that this rotation is responsible for effector secretion. To observe T3SA rotation, we constructed a novel observation system by modifying the tip of T3SA on bacterial cell membranes with an observation probe, which allowed documentation of T3SA rotation for the first time. T3SA rotation was stopped by the addition of a protonophore that decreases PMF. Moreover, increased viscosity of the observation medium inhibited both rotation of T3SA associated with beads and effector secretion. These results suggested that effector secretion would follow the PMF-dependent rotation of T3SA and could be inhibited by preventing T3SA rotation. Moreover, the motion-track analysis of bead rotation suggested that the T3SA needle might be flexible. Consequently, we propose a “rotational secretion model” as a novel effector secretion mechanism of T3SA.
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Searching algorithm for type IV secretion system effectors 1.0: a tool for predicting type IV effectors and exploring their genomic context

Type IV effectors (T4Es) are proteins produced by pathogenic bacteria to manipulate host cell gene expression and processes, divert the cell machinery for their own profit and circumvent the immune responses. T4Es have been characterized for some bacteria but many remain to be discovered. To help biologists identify putative T4Es from the complete genome of α- and γ-proteobacteria, we developed a Perl-based command line bioinformatics tool called S4TE (searching algorithm for type-IV secretion system effectors). The tool predicts and ranks T4E candidates by using a combination of 13 sequence characteristics, including homology to known effectors, homology to eukaryotic domains, presence of subcellular localization signals or secretion signals, etc. S4TE software is modular, and specific motif searches are run independently before ultimate combination of the outputs to generate a score and sort the strongest T4Es candidates. The user keeps the possibility to adjust various searching parameters such as the weight of each module, the selection threshold or the input databases. The algorithm also provides a GC% and local gene density analysis, which strengthen the selection of T4E candidates. S4TE is a unique predicting tool for T4Es, finding its utility upstream from experimental biology.
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Unique tool to predict Type IV effectors
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PLOS ONE: An Improved Method for TAL Effectors DNA-Binding Sites Prediction Reveals Functional Convergence in TAL Repertoires of Xanthomonas oryzae Strains

PLOS ONE: An Improved Method for TAL Effectors DNA-Binding Sites Prediction Reveals Functional Convergence in TAL Repertoires of Xanthomonas oryzae Strains | Effectors | Scoop.it
PLOS ONE: an inclusive, peer-reviewed, open-access resource from the PUBLIC LIBRARY OF SCIENCE. Reports of well-performed scientific studies from all disciplines freely available to the whole world.
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