Effectors & Plant immunity
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Rescooped by Maofeng Jing from Plants and Microbes
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Science: Nuclear-localized cyclic nucleotide–gated channels mediate symbiotic calcium oscillations (2016)

Science: Nuclear-localized cyclic nucleotide–gated channels mediate symbiotic calcium oscillations (2016) | Effectors & Plant immunity | Scoop.it

Nuclear-associated Ca2+ oscillations mediate plant responses to beneficial microbial partners—namely, nitrogen-fixing rhizobial bacteria that colonize roots of legumes and arbuscular mycorrhizal fungi that colonize roots of the majority of plant species. A potassium-permeable channel is known to be required for symbiotic Ca2+ oscillations, but the calcium channels themselves have been unknown until now. We show that three cyclic nucleotide–gated channels in Medicago truncatula are required for nuclear Ca2+ oscillations and subsequent symbiotic responses. These cyclic nucleotide–gated channels are located at the nuclear envelope and are permeable to Ca2+. We demonstrate that the cyclic nucleotide–gated channels form a complex with the postassium-permeable channel, which modulates nuclear Ca2+ release. These channels, like their counterparts in animal cells, might regulate multiple nuclear Ca2+ responses to developmental and environmental conditions.


Via Jean-Michel Ané, Kamoun Lab @ TSL
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Classification of cell death: How do cells die?

Classification of cell death: How do cells die? | Effectors & Plant immunity | Scoop.it
Cell death can be classified according to its morphological appearance (which may be apoptotic, necrotic, autophagic or associated with mitosis), enzymological criteria (with and without the involvement of nucleases or of distinct classes of proteases, such as caspases, calpains, cathepsins and transglutaminases), functional aspects (programmed or accidental, physiological or pathological) or immunological characteristics (immunogenic or non-immunogenic). The Nomenclature Committee on Cell Death (NCCD) has formulated a first round of recommendations in 2005, in Cell Death and Differentiation. Since then, the field of cell death research has continued its expansion, significant progress has been made and new putative cell death modalities have been described. The NCCD provides a forum in which names describing distinct modalities of cell death are critically evaluated and recommendations on their definition and use are formulated, hoping that a non-rigid, yet uniform, nomenclature will facilitate the communication among scientists and ultimately accelerate the pace of discovery. As it stands now, three distinct routes of cellular catabolism can be defined according to morphological criteria, namely apoptosis (which is a form of cell death), autophagy (which causes the destruction of a part of the cytoplasm, but mostly avoids cell death) and necrosis (which is another form of cell death). Although frequently employed in the past, the use of Roman numerals (i.e., type I, type II and type III cell death, respectively) to indicate these catabolic processes should be abandoned. Moreover, several critiques can be formulated against the clear-cut distinction of different cell types in the triad of apoptosis, autophagic cell death and necrosis. First, although this vocabulary was originally introduced based on observations of developing animals, it has rapidly been adopted to describe the results of in vitro studies performed on immortalized cell lines, which reflect very poorly the physiology of cell death in vivo. In tissues, indeed, dying cells are usually engulfed well before signs of advanced apoptosis or necrosis become detectable. Thus, it may be acceptable - if the irreversibility of these phenomena is demonstrated - to assess caspase activation and/or DNA fragmentation to diagnose apoptotic cell death in vivo. Second, there are numerous examples in which cell death displays mixed features, for instance with signs of both apoptosis and necrosis, a fact that lead to the introduction of terms like ‘necroapoptosis’ and ‘aponecrosis’ (whose use is discouraged by the NCCD to avoid further confusion). Similarly, in the involuting D. melanogaster salivary gland, autophagic vacuolization is synchronized with signs of apoptosis, and results from genetic studies indicate that caspases and autophagy act in an additive manner to ensure cell death in this setting. Altogether, these data argue against a clear-cut and absolute distinction between different forms of cell death based on morphological criteria. Third (and most important), it would be a desideratum to replace morphological aspects with biochemical/functional criteria to classify cell death modalities. Unfortunately, there is no clear equivalence between morphology and biochemistry, suggesting that the ancient morphological terms are doomed to disappear and to be replaced by truly biochemical definitions. In this context, ‘loss-of-function’ and ‘gain-of function’ genetic approaches (e.g., RNA interference, knockout models and plasmid-driven overexpression systems) represent invaluable tools to characterize cell death modes with more precision, but only if such interventions truly reduce/augment the rate of death, instead of changing its morphological appearance (as it is often the case). Present cell death classifications are reminiscent of the categorization of tumors that has been elaborated by pathologists over the last one and a half centuries. As old morphological categorizations of tumors are being more and more supported (and will presumably be replaced) by molecular diagnostics (which allows for a more sophisticated stratification of cancer subtypes based on molecular criteria), the current catalog of cell death types is destined to lose its value as compared with biochemical/functional tests. In the end, such efforts of classification are only justified when they have a prognostic and/or predictive impact, allowing the matching of each individual cancer with the appropriate therapy. Similarly, a cell death nomenclature will be considered useful only if it predicts the possibilities to pharmacologically/genetically modulate (induce or inhibit) cell death and/or if it predicts the consequences of cell death in vivo, with regard to inflammation and recognition by the immune system.
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Plant Journal: Wheat PR-1 proteins are targeted by necrotrophic pathogen effector proteins (2016)

Plant Journal: Wheat PR-1 proteins are targeted by necrotrophic pathogen effector proteins (2016) | Effectors & Plant immunity | Scoop.it

Recent studies have identified that proteinaceous effectors secreted by Parastagonospora nodorum are required to cause disease on wheat. These effectors interact in a gene-for-gene manner with host dominant susceptibilty loci, resulting in disease. However, whilst the requirement of these effectors for infection is clear, their mechanisms of action remain poorly understood. A yeast-two-hybrid library approach was used to search for wheat proteins that interacted with the necrotrophic effector SnTox3. Using this strategy we indentified an interaction between SnTox3 and the wheat pathogenicity-related protein TaPR-1-1, and confirmed it by in-planta co-immunprecipitation. PR-1 proteins represent a large family (23 in wheat) of proteins that are up-regulated early in the defence response, however their function remains ellusive. Interestingly, the P. nodorum effector SnToxA has recently been shown to interact specifically with TaPR-1-5. Our analysis of the SnTox3-TaPR-1 interaction demonstrated that SnTox3 can interact with a broader range of TaPR-1 proteins. Based on these data we utilised homology modeling to predict, and validate, regions on TaPR-1 proteins that are likely to be involved in the SnTox3 interaction. Precipitating from this work, we identified that a PR-1 derived defence signalling peptide from the C-terminus of TaPR1-1, known as CAPE1, enhanced the infection of wheat by P. nodorum in an SnTox3-dependent manner, but played no role in ToxA-mediated disease. Collectively, our data suggest that P.nodorum has evolved unique effectors that target a common host-protein involved in host defence, albeit with different mechanisms and potentially outcomes.


Via Kamoun Lab @ TSL
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PNAS: Phytophthora effector targets a novel component of small RNA pathway in plants to promote infection (2015)

PNAS: Phytophthora effector targets a novel component of small RNA pathway in plants to promote infection (2015) | Effectors & Plant immunity | Scoop.it

Phytophthora is a major threat to agriculture. However, the molecular interaction of these severe pathogens with plant hosts is poorly understood. Here, we report that the Phytophthora Suppressor of RNA Silencing 1 (PSR1) effectively promotes infection in Arabidopsis thaliana by directly targeting an essential protein containing a aspartate–glutamate–alanine–histidine-box RNA helicase domain. This PSR1-Interacting Protein 1 (PINP1) is required for the accumulation of distinct classes of endogenous small RNAs and acts as a positive regulator of plant immunity. Silencing of PINP1 impaired the assembly of microRNA-processing complexes in the nucleus, leading to defects in development and immunity. This study revealed a conserved RNA helicase as a regulator of RNA silencing and provides mechanistic insight into Phytophthora pathogenesis.


Via Kamoun Lab @ TSL
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Plant Cell: A Secreted Effector Protein of Ustilago maydis Guides Maize Leaf Cells to Form Tumors (2015)

Plant Cell: A Secreted Effector Protein of Ustilago maydis Guides Maize Leaf Cells to Form Tumors (2015) | Effectors & Plant immunity | Scoop.it

The biotrophic smut fungus Ustilago maydis infects all aerial organs of maize (Zea mays) and induces tumors in the plant tissues. U. maydis deploys many effector proteins to manipulate its host. Previously, deletion analysis demonstrated that several effectors have important functions in inducing tumor expansion specifically in maize leaves. Here, we present the functional characterization of the effector See1 (Seedling efficient effector1). See1 is required for the reactivation of plant DNA synthesis, which is crucial for tumor progression in leaf cells. By contrast, See1 does not affect tumor formation in immature tassel floral tissues, where maize cell proliferation occurs independent of fungal infection. See1 interacts with a maize homolog of SGT1 (Suppressor of G2 allele of skp1), a factor acting in cell cycle progression in yeast (Saccharomyces cerevisiae) and an important component of plant and human innate immunity. See1 interferes with the MAPK-triggered phosphorylation of maize SGT1 at a monocot-specific phosphorylation site. We propose that See1 interferes with SGT1 activity, resulting in both modulation of immune responses and reactivation of DNA synthesis in leaf cells. This identifies See1 as a fungal effector that directly and specifically contributes to the formation of leaf tumors in maize.


Via Kamoun Lab @ TSL
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New Phytologist: The AVR2–SIX5 gene pair is required to activate I-2-mediated immunity in tomato (2015)

New Phytologist: The AVR2–SIX5 gene pair is required to activate I-2-mediated immunity in tomato (2015) | Effectors & Plant immunity | Scoop.it
Plant-invading microbes betray their presence to a plant by exposure of antigenic molecules such as small, secreted proteins called ‘effectors’. In Fusarium oxysporum f. sp. lycopersici (Fol) we identified a pair of effector gene candidates, AVR2-SIX5, whose expression is controlled by a shared promoter.The pathogenicity of AVR2 and SIX5 Fol knockouts was assessed on susceptible and resistant tomato (Solanum lycopersicum) plants carrying I-2. The I-2 NB-LRR protein confers resistance to Fol races carrying AVR2.Like Avr2, Six5 was found to be required for full virulence on susceptible plants. Unexpectedly, each knockout could breach I-2-mediated disease resistance. So whereas Avr2 is sufficient to induce I-2-mediated cell death, Avr2 and Six5 are both required for resistance. Avr2 and Six5 interact in yeast two-hybrid assays as well as in planta. Six5 and Avr2 accumulate in xylem sap of plants infected with the reciprocal knockouts, showing that lack of I-2 activation is not due to a lack of Avr2 accumulation in the SIX5 mutant.The effector repertoire of a pathogen determines its host specificity and its ability to manipulate plant immunity. Our findings challenge an oversimplified interpretation of the gene-for-gene model by showing requirement of two fungal genes for immunity conferred by one resistance gene.
Via Kamoun Lab @ TSL
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PNAS: Plant-derived antifungal agent poacic acid targets β-1,3-glucan (2015)

PNAS: Plant-derived antifungal agent poacic acid targets β-1,3-glucan (2015) | Effectors & Plant immunity | Scoop.it

A rise in resistance to current antifungals necessitates strategies to identify alternative sources of effective fungicides. We report the discovery of poacic acid, a potent antifungal compound found in lignocellulosic hydrolysates of grasses. Chemical genomics using Saccharomyces cerevisiae showed that loss of cell wall synthesis and maintenance genes conferred increased sensitivity to poacic acid. Morphological analysis revealed that cells treated with poacic acid behaved similarly to cells treated with other cell wall-targeting drugs and mutants with deletions in genes involved in processes related to cell wall biogenesis. Poacic acid causes rapid cell lysis and is synergistic with caspofungin and fluconazole. The cellular target was identified; poacic acid localized to the cell wall and inhibited β-1,3-glucan synthesis in vivo and in vitro, apparently by directly binding β-1,3-glucan. Through its activity on the glucan layer, poacic acid inhibits growth of the fungi Sclerotinia sclerotiorum and Alternaria solani as well as the oomycete Phytophthora sojae. A single application of poacic acid to leaves infected with the broad-range fungal pathogen S. sclerotiorumsubstantially reduced lesion development. The discovery of poacic acid as a natural antifungal agent targeting β-1,3-glucan highlights the potential side use of products generated in the processing of renewable biomass toward biofuels as a source of valuable bioactive compounds and further clarifies the nature and mechanism of fermentation inhibitors found in lignocellulosic hydrolysates.


Via Kamoun Lab @ TSL
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Steve Marek's curator insight, June 1, 2015 10:33 AM

Nice study using yeast genetics to identify mode of action of cell wall compound from grasses; with implications for cellulosic biofuel production.

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Microbiology and Molecular Biology Reviews: Oomycete Interactions with Plants: Infection Strategies and Resistance Principles (2015)

Microbiology and Molecular Biology Reviews: Oomycete Interactions with Plants: Infection Strategies and Resistance Principles (2015) | Effectors & Plant immunity | Scoop.it

The Oomycota include many economically significant microbial pathogens of crop species. Understanding the mechanisms by which oomycetes infect plants and identifying methods to provide durable resistance are major research goals. Over the last few years, many elicitors that trigger plant immunity have been identified, as well as host genes that mediate susceptibility to oomycete pathogens. The mechanisms behind these processes have subsequently been investigated and many new discoveries made, marking a period of exciting research in the oomycete pathology field. This review provides an introduction to our current knowledge of the pathogenic mechanisms used by oomycetes, including elicitors and effectors, plus an overview of the major principles of host resistance: the established R gene hypothesis and the more recently defined susceptibility (S) gene model. Future directions for development of oomycete-resistant plants are discussed, along with ways that recent discoveries in the field of oomycete-plant interactions are generating novel means of studying how pathogen and symbiont colonizations overlap.


Via Kamoun Lab @ TSL
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Quantitative Peptidomics Study Reveals That a Wound-Induced Peptide from PR-1 Regulates Immune Signaling in Tomato

Many important cell-to-cell communication events in multicellular organisms are mediated by peptides, but only a few peptides have been identified in plants. In an attempt to address the difficulties in identifying plant signaling peptides, we developed a novel peptidomics approach and used this approach to discover defense signaling peptides in plants. In addition to the canonical peptide systemin, several novel peptides were confidently identified in tomato (Solanum lycopersicum) and quantified to be induced by both wounding and methyl jasmonate (MeJA). A wounding or wounding plus MeJA-induced peptide derived from the pathogenesis-related protein 1 (PR-1) family was found to induce significant antipathogen and minor antiherbivore responses in tomato. This study highlights a role for PR-1 in immune signaling and suggests the potential application of plant endogenous peptides in efforts to defeat biological threats in crop production. As PR-1 is highly conserved across many organisms and the putative peptide from At-PR1 was also found to be bioactive in Arabidopsis thaliana, our results suggest that this peptide may be useful for enhancing resistance to stress in other plant species.


Via Guogen Yang
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Small regulatory RNAs and the fine-tuning of plant–bacteria interactions

Small regulatory RNAs and the fine-tuning of plant–bacteria interactions | Effectors & Plant immunity | Scoop.it
Small regulatory RNAs (sRNAs) play a key role in many physiological and adaptive responses in bacteria. Faced with rapidly changing environments, it is more advantageous for bacteria to use sRNA-mediated responses than regulation by protein transcriptional factors, as sRNAs act at the post-transcriptional level and require less energy and time for their synthesis and turnover. The use of RNA deep sequencing has provided hundreds of sRNA candidates in different bacterial species that interact with plants. Here, we review the most recent results for the involvement of bacterial sRNAs in beneficial as well as deleterious plant–bacteria interactions. We describe the current view for the role of sRNAs, which are suggested to improve competition for both niches and resources in plant-interacting bacteria. These sRNAs also help plant-associated bacteria individually adapt to the rapidly changing conditions to which they are exposed, during different stages of this interaction.

Via Jean-Michel Ané, Guogen Yang
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Carbohydrates in plant immunity and plant protection: roles and potential application as foliar sprays

Carbohydrates in plant immunity and plant protection: roles and potential application as foliar sprays | Effectors & Plant immunity | Scoop.it
Increasing interest is devoted to carbohydrates for their roles in plant immunity. Some of them are elicitors of plant defenses whereas other ones act as signaling molecules in a manner similar to phytohormones. This review first describes the main classes of carbohydrates associated to plant immunity, their role and mode of action. More precisely, the state of the art about perception of “PAMP, MAMP, and DAMP (Pathogen-, Microbe-, Damage-Associated Molecular Patterns) type” oligosaccharides is presented and examples of induced defense events are provided. A particular attention is paid to the structure/activity relationships of these compounds. The role of sugars as signaling molecules, especially in plant microbe interactions, is also presented. Secondly, the potentialities and limits of foliar sprays of carbohydrates to stimulate plant immunity for crop protection against diseases are discussed, with focus on the roles of the leaf cuticle and phyllosphere microflora.

Via Christophe Jacquet, Guogen Yang
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Fungal Genetics and Biology: The Podosphaera xanthii haustorium, the fungal Trojan horse of cucurbit-powdery mildew interactions (2014)

Fungal Genetics and Biology: The Podosphaera xanthii haustorium, the fungal Trojan horse of cucurbit-powdery mildew interactions (2014) | Effectors & Plant immunity | Scoop.it

The powdery mildew fungi are obligate biotrophic plant pathogens that develop a specialized structure for parasitism termed haustorium, which is responsible for nutrient uptake and factor exchange with the plant. In this work, we present a detailed microscopy analysis of the haustoria of the cucurbit powdery mildew fungus Podosphaera xanthii, a major limiting factor for cucurbit production worldwide. Despite being located inside plant epidermal cells, transmission electron microscopy (TEM) analysis showed the characteristic highly irregular outline of the extrahaustorial membrane that separates the extrahaustorial matrix of haustoria from the cytoplasm of the plant cell. TEM analysis also revealed the presence of some vesicles and electron-dense plaques of material surrounding the haustoria. In confocal microscopy analysis and aniline blue staining we found a positive correlation between haustorial development and deposition of callose, which is distributed as plaques around haustorial complex. In this study, a method for the isolation of P. xanthii haustoria was also adapted, which permitted the analysis of the formation of haustorial lobes and the visualization of vacuoles and the pool of vesicles inside the haustorial complex. Our findings suggested that the haustorial lobes were responsible for vesicular trafficking and most likely act as the main mediators of the fungus-plant dialogue. All of these findings were integrated into a model of the P. xanthii-host cellular interactions.


Via Kamoun Lab @ TSL
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PLOS Pathogens: Expression Profiling during Arabidopsis/Downy Mildew Interaction Reveals a Highly-Expressed Effector That Attenuates Responses to Salicylic Acid (2014)

PLOS Pathogens: Expression Profiling during Arabidopsis/Downy Mildew Interaction Reveals a Highly-Expressed Effector That Attenuates Responses to Salicylic Acid (2014) | Effectors & Plant immunity | Scoop.it

Plants have evolved strong innate immunity mechanisms, but successful pathogens evade or suppress plant immunity via effectors delivered into the plant cell. Hyaloperonospora arabidopsidis (Hpa) causes downy mildew on Arabidopsis thaliana, and a genome sequence is available for isolate Emoy2. Here, we exploit the availability of genome sequences for Hpa and Arabidopsis to measure gene-expression changes in both Hpa and Arabidopsis simultaneously during infection. Using a high-throughput cDNA tag sequencing method, we reveal expression patterns of Hpa predicted effectors and Arabidopsis genes in compatible and incompatible interactions, and promoter elements associated with Hpa genes expressed during infection. By resequencing Hpa isolate Waco9, we found it evades Arabidopsis resistance gene RPP1through deletion of the cognate recognized effector ATR1. Arabidopsis salicylic acid (SA)-responsive genes including PR1 were activated not only at early time points in the incompatible interaction but also at late time points in the compatible interaction. By histochemical analysis, we found that Hpa suppresses SA-inducible PR1 expression, specifically in the haustoriated cells into which host-translocated effectors are delivered, but not in non-haustoriated adjacent cells. Finally, we found a highly-expressed Hpa effector candidate that suppresses responsiveness to SA. As this approach can be easily applied to host-pathogen interactions for which both host and pathogen genome sequences are available, this work opens the door towards transcriptome studies in infection biology that should help unravel pathogen infection strategies and the mechanisms by which host defense responses are overcome.


Via Kamoun Lab @ TSL
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Annual Review of Phytopathology: Cladosporium fulvum Effectors: Weapons in the Arms Race with Tomato (2016)

Annual Review of Phytopathology: Cladosporium fulvum Effectors: Weapons in the Arms Race with Tomato (2016) | Effectors & Plant immunity | Scoop.it

In this review, I recount my personal history. My drive to study host-pathogen interactions was to find alternatives for agrochemicals, which was triggered after reading the book “Silent Spring” by Rachel Carson. I reflect on my research at the Laboratory of Phytopathology at Wageningen University, where I have worked for my entire career on the interaction between Cladosporium fulvum and tomato, and related gene-for-gene pathosystems. I describe different methods used to identify and sequence avirulence (Avr) genes from the pathogen and resistance (R) genes from the host. The major genes involved in classical gene-for-gene interactions have now been identified, and breeders can produce plants with multiple R genes providing durable and environmentally safe protection against pathogens. In some cases, this might require the use of genetically modified plants when R genes cannot be introduced by classical breeding.


Via Kamoun Lab @ TSL
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Molecular Mechanisms Underlying the Autophagy Processing in Cell, March 2013

All Rights Are Reserved. For any use of this video, please contact me at malireza@scripps.edu Thank you Acknowledgment: Dr. Lindsay Whitton, my mentor. Dr. M...

Via Jeff Keyser
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Nature Communications : A Phytophthora sojae effector suppresses endoplasmic reticulum stress-mediated immunity by stabilizing plant Binding immunoglobulin Proteins 

Nature Communications : A Phytophthora sojae effector suppresses endoplasmic reticulum stress-mediated immunity by stabilizing plant Binding immunoglobulin Proteins  | Effectors & Plant immunity | Scoop.it
Phytophthora pathogens secrete an array of specific effector proteins to manipulate host innate immunity to promote pathogen colonization. However, little is known about the host targets of effectors and the specific mechanisms by which effectors increase susceptibility. Here we report that the soybean pathogen Phytophthora sojae uses an essential effector PsAvh262 to stabilize endoplasmic reticulum (ER)-luminal binding immunoglobulin proteins (BiPs), which act as negative regulators of plant resistance to Phytophthora. By stabilizing BiPs, PsAvh262 suppresses ER stress-triggered cell death and facilitates Phytophthora infection. The direct targeting of ER stress regulators may represent a common mechanism of host manipulation by microbes.
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Welcome to 4ICBPI ! The 4th International Conference on Biotic Plant Interactions, Nanjing, Jiangsu, China, on Aug 1-3, 2015.

Welcome to 4ICBPI ! The 4th International Conference on Biotic Plant Interactions,  Nanjing, Jiangsu, China, on Aug 1-3, 2015. | Effectors & Plant immunity | Scoop.it
Maofeng Jing's insight:

Plants constantly interact with a wide range of microbes and insects. These interactions, which can be beneficial or harmful to plants, influence greatly on agricultural production and our daily life. On behalf of the steering committee, it is our pleasure to invite colleagues in the fields of biotic plant interactions to attend the 4th International Conference on Biotic Plant Interactions, which will be held at Nanjing, Jiangsu, China, on Aug 1-3, 2015.

The theme of this 3-day meeting is Biotic Plant Interactions and Agricultural Production. As a continuing effort after the 1st conference held in Brisbane, Australia, 2008, 2nd conference held in Kunming, China, 2011, and 3rd conference held in Yangling, China, 2013, this meeting will cover a wide range of scientific research topics spanning Plant Pathology, Plant-Microbe Interactions, Plant-Insect interactions, Pathogen and Insect Genomics and Molecular Evolution, and Biotechnology on disease and insect resistance. This conference will bring together scientists and students who are interested in plant pathology and beneficial interactions of plants with other organisms, including viruses, bacteria, fungi, oomycetes, nematodes, insects and other herbivores, and genomics and evolution of pathogens and insects.

We are looking forward to welcoming you in Nanjing, China.

Sincerely Yours!

Yuanchao Wang & Zuhua He

Chairmans of the Organizing Committee 

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Developmental Cell: Chloroplast Stromules Function during Innate Immunity (2015)

Developmental Cell: Chloroplast Stromules Function during Innate Immunity (2015) | Effectors & Plant immunity | Scoop.it

Chloroplast stromules are induced during plant immune responsesPro-PCD signals such as SA and H2O2 induce stromulesStromules form dynamic connections with nucleus during immune responsesConstitutively induced stromules enhance PCD during plant immune responses

 

Inter-organellar communication is vital for successful innate immune responses that confer defense against pathogens. However, little is known about how chloroplasts, which are a major production site of pro-defense molecules, communicate and coordinate with other organelles during defense. Here we show that chloroplasts send out dynamic tubular extensions called stromules during innate immunity or exogenous application of the pro-defense signals, hydrogen peroxide (H2O2) and salicylic acid. Interestingly, numerous stromules surround nuclei during defense response, and these connections correlate with an accumulation of chloroplast-localized NRIP1 defense protein and H2O2 in the nucleus. Furthermore, silencing and knockout of chloroplast unusual positioning 1 (CHUP1) that encodes a chloroplast outer envelope protein constitutively induces stromules in the absence of pathogen infection and enhances programmed cell death. These results support a model in which stromules aid in the amplification and/or transport of pro-defense signals into the nucleus and other subcellular compartments during immunity.


Via Kamoun Lab @ TSL, Guogen Yang
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mmatshepo sibuyi's curator insight, July 31, 2015 4:49 AM

chloroplast consist of green pigments called chlorophyll that plants use in the process of photosynthesis

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Cell: A Receptor Pair with an Integrated Decoy Converts Pathogen Disabling of Transcription Factors to Immunity (2015)

Cell: A Receptor Pair with an Integrated Decoy Converts Pathogen Disabling of Transcription Factors to Immunity (2015) | Effectors & Plant immunity | Scoop.it

Microbial pathogens infect host cells by delivering virulence factors (effectors) that interfere with defenses. In plants, intracellular nucleotide-binding/leucine-rich repeat receptors (NLRs) detect specific effector interference and trigger immunity by an unknown mechanism. The Arabidopsis-interacting NLR pair, RRS1-R with RPS4, confers resistance to different pathogens, including Ralstonia solanacearum bacteria expressing the acetyltransferase effector PopP2. We show that PopP2 directly acetylates a key lysine within an additional C-terminal WRKY transcription factor domain of RRS1-R that binds DNA. This disrupts RRS1-R DNA association and activates RPS4-dependent immunity. PopP2 uses the same lysine acetylation strategy to target multiple defense-promoting WRKY transcription factors, causing loss of WRKY-DNA binding and transactivating functions needed for defense gene expression and disease resistance. Thus, RRS1-R integrates an effector target with an NLR complex at the DNA to switch a potent bacterial virulence activity into defense gene activation.

 


Via Freddy Monteiro, Christophe Jacquet, DrDrPlant, Kamoun Lab @ TSL
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Freddy Monteiro's curator insight, May 21, 2015 12:55 PM

See also the back-to-back paper:

A Plant Immune Receptor Detects Pathogen Effectors that Target WRKY Transcription Factors. www.cell.com/cell/abstract/S0092-8674(15)00441-9

 

See also the preview:

Treasure Your Exceptions: Unusual Domains in Immune Receptors Reveal Host Virulence Targets. http://www.cell.com/cell/abstract/S0092-8674%2815%2900566-8

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Current Opinion in Plant Biology: Regulation of appressorium development in pathogenic fungi (2015)

Current Opinion in Plant Biology: Regulation of appressorium development in pathogenic fungi (2015) | Effectors & Plant immunity | Scoop.it

• Appressorium development is linked to cell cycle checkpoints controlling morphogenesis.
• Ras GTPase signalling acts upstream of cAMP and MAP kinase pathways for appressorium development.
• Melanin is not exclusively associated with appressorium turgor generation.
• Septin-mediated actin re-modelling is essential for appressorium function.
• Focal secretion of effectors occurs during appressorium infection.

Many plant pathogenic fungi have the capacity to breach the intact cuticles of their plant hosts using specialised infection cells called appressoria. These cells exert physical force to rupture the plant surface, or deploy enzymes in a focused way to digest the cuticle and plant cell wall. They also provide the means by which focal secretion of effectors occurs at the point of plant infection. Development of appressoria is linked to re-modelling of the actin cytoskeleton, mediated by septin GTPases, and rapid cell wall differentiation. These processes are regulated by perception of plant cell surface components, and starvation stress, but also linked to cell cycle checkpoints that control the overall progression of infection-related development.


Via Christophe Jacquet, Francis Martin, Kamoun Lab @ TSL
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Frontiers | Interactions of Xanthomonas type-III effector proteins with the plant ubiquitin and ubiquitin-like pathways | Plant-Microbe Interaction

Frontiers | Interactions of Xanthomonas type-III effector proteins with the plant ubiquitin and ubiquitin-like pathways | Plant-Microbe Interaction | Effectors & Plant immunity | Scoop.it
In eukaryotes, regulated protein turnover is required during many cellular processes, including defense against pathogens. Ubiquitination and degradation of ubiquitinated proteins via the ubiquitin – proteasome system (UPS) is the main pathway for the turnover of intracellular proteins in eukaryotes. The extensive utilization of the UPS in host cells makes it an ideal pivot for the manipulation of cellular processes by pathogens. Like many other Gram-negative bacteria, Xanthomonas species secrete a suite of type-III effector proteins (T3Es) into their host cells to promote virulence. Some of these T3Es exploit the plant UPS to interfere with immunity. This review summarizes T3E examples from the genus Xanthomonas with a proven or suggested interaction with the host UPS or UPS-like systems and also discusses the apparent paradox that arises from the presence of T3Es that inhibit the UPS in general while others rely on its activity for their function.

Via Suayib Üstün, Guogen Yang
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Suayib Üstün's curator insight, December 3, 2014 8:19 AM

My first Review is online! Also first paper in Frontiers in Plant Science. Next one in this issue is following soon...

Jennifer Mach's comment, December 3, 2014 8:56 AM
Congratulations!
Rescooped by Maofeng Jing from Plant-Microbe Interaction
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Promoter-Based Integration in Plant Defense Regulation

Promoter-Based Integration in Plant Defense Regulation | Effectors & Plant immunity | Scoop.it
A key unanswered question in plant biology is how a plant regulates metabolism to maximize performance across an array of biotic and abiotic environmental stresses. In this study, we addressed the potential breadth of transcriptional regulation that can alter accumulation of the defensive glucosinolate metabolites in Arabidopsis (Arabidopsis thaliana). A systematic yeast one-hybrid study was used to identify hundreds of unique potential regulatory interactions with a nearly complete complement of 21 promoters for the aliphatic glucosinolate pathway. Conducting high-throughput phenotypic validation, we showed that >75% of tested transcription factor (TF) mutants significantly altered the accumulation of the defensive glucosinolates. These glucosinolate phenotypes were conditional upon the environment and tissue type, suggesting that these TFs may allow the plant to tune its defenses to the local environment. Furthermore, the pattern of TF/promoter interactions could partially explain mutant phenotypes. This work shows that defense chemistry within Arabidopsis has a highly intricate transcriptional regulatory system that may allow for the optimization of defense metabolite accumulation across a broad array of environments.

Via Christophe Jacquet, Guogen Yang
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Rescooped by Maofeng Jing from Plant-Microbe Interaction
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A Noncanonical Role for the CKI-RB-E2F Cell-Cycle Signaling Pathway in Plant Effector-Triggered Immunity

A Noncanonical Role for the CKI-RB-E2F Cell-Cycle Signaling Pathway in Plant Effector-Triggered Immunity | Effectors & Plant immunity | Scoop.it
Highlights



The nuclear membrane protein CPR5 inhibits effector-triggered immunity (ETI)


CPR5 inhibits ETI via interaction with cyclin-dependent kinase inhibitors (CKIs)


CKIs are released from CPR5 upon ETI induction and are required for PCD and immunity


CKIs induce immunity through RB hyperphosphorylation and E2F overactivation

Summary

Effector-triggered immunity (ETI), the major host defense mechanism in plants, is often associated with programmed cell death (PCD). Plants lack close homologs of caspases, the key mediators of PCD in animals. So although the NB-LRR receptors involved in ETI are well studied, how they activate PCD and confer disease resistance remains elusive. We show that the Arabidopsis nuclear envelope protein, CPR5, negatively regulates ETI and the associated PCD through a physical interaction with cyclin-dependent kinase inhibitors (CKIs). Upon ETI induction, CKIs are released from CPR5 to cause overactivation of another core cell-cycle regulator, E2F. In cki and e2f mutants, ETI responses induced by both TIR-NB-LRR and CC-NB-LRR classes of immune receptors are compromised. We further show that E2F is deregulated during ETI, probably through CKI-mediated hyperphosphorylation of retinoblastoma-related 1 (RBR1). This study demonstrates that canonical cell-cycle regulators also play important noncanonical roles in plant immunity.

Via Christophe Jacquet, Guogen Yang
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Rescooped by Maofeng Jing from Plants and Microbes
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Nature Communications: Long-distance endosome trafficking drives fungal effector production during plant infection (2014)

Nature Communications: Long-distance endosome trafficking drives fungal effector production during plant infection (2014) | Effectors & Plant immunity | Scoop.it

To cause plant disease, pathogenic fungi can secrete effector proteins into plant cells to suppress plant immunity and facilitate fungal infection. Most fungal pathogens infect plants using very long strand-like cells, called hyphae, that secrete effectors from their tips into host tissue. How fungi undergo long-distance cell signalling to regulate effector production during infection is not known. Here we show that long-distance retrograde motility of early endosomes (EEs) is necessary to trigger transcription of effector-encoding genes during plant infection by the pathogenic fungus Ustilago maydis. We demonstrate that motor-dependent retrograde EE motility is necessary for regulation of effector production and secretion during host cell invasion. We further show that retrograde signalling involves the mitogen-activated kinase Crk1 that travels on EEs and participates in control of effector production. Fungal pathogens therefore undergo long-range signalling to orchestrate host invasion.


Via Kamoun Lab @ TSL
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Rescooped by Maofeng Jing from Plants and Microbes
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Cell Host & Microbe: A Plant Phosphoswitch Platform Repeatedly Targeted by Type III Effector Proteins Regulates the Output of Both Tiers of Plant Immune Receptors (2014)

Cell Host & Microbe: A Plant Phosphoswitch Platform Repeatedly Targeted by Type III Effector Proteins Regulates the Output of Both Tiers of Plant Immune Receptors (2014) | Effectors & Plant immunity | Scoop.it

Plants detect microbes via two functionally interconnected tiers of immune receptors. Immune detection is suppressed by equally complex pathogen mechanisms. The small plasma-membrane-tethered protein RIN4 negatively regulates microbe-associated molecular pattern (MAMP)-triggered responses, which are derepressed upon bacterial flagellin perception. We demonstrate that recognition of the flagellin peptide MAMP flg22 triggers accumulation of RIN4 phosphorylated at serine 141 (pS141) that mediates derepression of several immune outputs. RIN4 is targeted by four bacterial type III effector proteins, delivered temporally after flagellin perception. Of these, AvrB acts with a host kinase to increase levels of RIN4 phosphorylated at threonine 166 (pT166). RIN4 pT166 is epistatic to RIN4 pS141. Thus, AvrB contributes to virulence by enhancing “rerepression” of immune system outputs. Our results explain the evolution of independent effectors that antagonize accumulation of RIN4 pS141 and of a specific plant intracellular NLR protein, RPM1, which is activated by AvrB-mediated accumulation of RIN4 pT166.


Via Kamoun Lab @ TSL
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