microbial pathogenesis and plant immunity
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A Bacterial Tyrosine Phosphatase Inhibits Plant Pattern Recognition Receptor Activation

A Bacterial Tyrosine Phosphatase Inhibits Plant Pattern Recognition Receptor Activation | microbial pathogenesis and plant immunity | Scoop.it

Scooped from: Science, 2014

Authors: Alberto P. Macho, Benjamin Schwessinger, Vardis Ntoukakis, Alexandre Brutus, Cécile Segonzac, Sonali Roy, Yasuhiro Kadota, Man-Ho Oh, Jan Sklenar, Paul Derbyshire, Rosa Lozano-Durán, Frederikke Gro Malinovsky, Jacqueline Monaghan, Frank L. Menke, Steven C. Huber, Sheng Yang He and Cyril Zipfel.

 

Summary: 

Innate immunity relies on the perception of pathogen-associated molecular patterns (PAMPs) by pattern-recognition receptors (PRRs) located on the host cell’s surface. Many plant PRRs are kinases. Here, we report that the Arabidopsis receptor kinase EF-TU RECEPTOR EFR, which perceives the elf18 peptide derived from bacterial elongation factor Tu, is activated upon ligand binding by phosphorylation on its tyrosine residues. Phosphorylation of a single tyrosine residue, Y836, is required for activation of EFR and downstream immunity to the phytopathogenic bacterium Pseudomonas syringae. A tyrosine phosphatase, HopAO1, secreted by P. syringae, reduces EFR phosphorylation and derails subsequent immune responses. Thus host and pathogen battle to take control of PRR tyrosine phosphorylation used to initiate anti-bacterial immunity.


Via Freddy Monteiro
Jim Alfano's insight:

Very interesting finding - A long sought target of the HopAO1 effector. HopAO1 also suppresses ETI - so additional targets remain undiscovered.

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Rescooped by Jim Alfano from Plant-Microbe Interactions
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PLOS Genetics: Differentiation between MAMP Triggered Defenses in Arabidopsis thaliana

PLOS Genetics: Differentiation between MAMP Triggered Defenses in  Arabidopsis thaliana | microbial pathogenesis and plant immunity | Scoop.it
Author Summary Specialized receptors encoded by plants detect different components of bacterial machinery, and initiate an immune response. These recognition events are thought to induce largely redundant defense signaling, the magnitude of which varies quantitatively among populations, perhaps in response to environment specific differences in microbial threat. Here, we sought to determine whether plants evolve distinct or shared responses to two canonical MAMPs within natural populations. We comprehensively tested the extent of functional redundancy in the response of 186 genotypes of Arabidopsis thaliana to variants of each of two classes of bacterial signals, flagellin and EF-Tu. Although plants respond similarly to recognition of different variants of the same MAMP, we found the response to one MAMP class to be largely uncorrelated with the response to the other class. We further investigated the genetic bases underlying growth changes to determine whether similar genes contribute to variation in the response to EF-Tu and flagellin bacterial signals. We find limited genetic similarity, revealing novel MAMP-specific signaling components. The differentiation of these responses reveals MAMP-specific fine tuning of the immune response.

Via Giannis Stringlis, Tatsuya Nobori
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Annu Rev Phytopathol: Plant Pathogen Effectors: Cellular Probes Interfering with Plant Defenses in Spatial and Temporal Manners

Annu Rev Phytopathol: Plant Pathogen Effectors: Cellular Probes Interfering with Plant Defenses in Spatial and Temporal Manners | microbial pathogenesis and plant immunity | Scoop.it

Via Tatsuya Nobori
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RNA ‘Information Warfare’ in Pathogenic and Mutualistic Interactions

RNA ‘Information Warfare’ in Pathogenic and Mutualistic Interactions | microbial pathogenesis and plant immunity | Scoop.it
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Via Tatsuya Nobori
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Genome Biology: Genomic screens identify a new phytobacterial microbe-associated molecular pattern and the cognate Arabidopsis receptor-like kinase that mediates its immune elicitation (2016)

Genome Biology: Genomic screens identify a new phytobacterial microbe-associated molecular pattern and the cognate Arabidopsis receptor-like kinase that mediates its immune elicitation (2016) | microbial pathogenesis and plant immunity | Scoop.it

Background - The recognition of microbe-associated molecular patterns during infection is central to the mounting of an effective immune response. In spite of their importance, it remains difficult to identify these molecules and the host receptors required for their perception, ultimately limiting our understanding of the role of these molecules in the evolution of host-pathogen relationships.

 

Results - We employ a comparative genomics screen to identify six new immune eliciting peptides from the phytopathogenic bacterium Pseudomonas syringae. We then perform a reverse genetic screen to identify Arabidopsis thaliana leucine-rich repeat receptor-like kinases required for the recognition of these elicitors. We test the six elicitors on 187 receptor-like kinase knock-down insertion lines using a high-throughput peroxidase-based immune assay and identify multiple lines that show decreased immune responses to specific peptides. From this primary screen data, we focused on the interaction between the xup25 peptide from a bacterial xanthine/uracil permease and the Arabidopsis receptor-like kinase xanthine/uracil permease sensing 1; a family XII protein closely related to two well-characterized receptor-like kinases. We show that xup25 treatment increases pathogenesis-related gene induction, callose deposition, seedling growth inhibition, and resistance to virulent bacteria, all in a xanthine/uracil permease sensing 1-dependent manner. Finally, we show that this kinase-like receptor can bind the xup25 peptide directly. These results identify xup25 as a P. syringae microbe-associated molecular pattern and xanthine/uracil permease sensing 1 as a receptor-like kinase that detects the xup25 epitope to activate immune responses.

 

Conclusions - The present study demonstrates an efficient method to identify immune elicitors and the plant receptors responsible for their perception. Further exploration of these molecules will increase our understanding of plant-pathogen interactions and the basis for host specificity.


Via Kamoun Lab @ TSL
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Scientific Reports: A Phytophthora sojae effector PsCRN63 forms homo-/hetero-dimers to suppress plant immunity via an inverted association manner (2016)

Scientific Reports: A Phytophthora sojae effector PsCRN63 forms homo-/hetero-dimers to suppress plant immunity via an inverted association manner (2016) | microbial pathogenesis and plant immunity | Scoop.it

Oomycete pathogens produce a large number of effectors to promote infection. Their mode of action are largely unknown. Here we show that a Phytophthora sojae effector, PsCRN63, suppresses flg22-induced expression of FRK1 gene, a molecular marker in pathogen-associated molecular patterns (PAMP)-triggered immunity (PTI). However, PsCRN63 does not suppress upstream signaling events including flg22-induced MAPK activation and BIK1 phosphorylation, indicating that it acts downstream of MAPK cascades. The PsCRN63-transgenic Arabidopsisplants showed increased susceptibility to bacterial pathogen Pseudomonas syringae pathovar tomato (Pst) DC3000 and oomycete pathogen Phytophthora capsici. The callose deposition were suppressed in PsCRN63-transgenic plants compared with the wild-type control plants. Genes involved in PTI were also down-regulated in PsCRN63-transgenic plants. Interestingly, we found that PsCRN63 forms an dimer that is mediated by inter-molecular interactions between N-terminal and C-terminal domains in an inverted association manner. Furthermore, the N-terminal and C-terminal domains required for the dimerization are widely conserved among CRN effectors, suggesting that homo-/hetero-dimerization of Phytophthora CRN effectors is required to exert biological functions. Indeed, the dimerization was required for PTI suppression and cell death-induction activities of PsCRN63.


Via Kamoun Lab @ TSL
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Mannitol in Plants, Fungi, and Plant–Fungal Interactions

Mannitol in Plants, Fungi, and Plant–Fungal Interactions | microbial pathogenesis and plant immunity | Scoop.it
Although the presence of mannitol in organisms as diverse as plants and fungi clearly suggests that this compound has important roles, our understanding of fungal mannitol metabolism and its interaction with mannitol metabolism in plants is far from complete. Despite recent inroads into understanding the importance of mannitol and its metabolic roles in salt, osmotic, and oxidative stress tolerance in plants and fungi, our current understanding of exactly how mannitol protects against reactive oxygen is also still incomplete. In this opinion, we propose a new model of the interface between mannitol metabolism in plants and fungi and how it impacts plant–pathogen interactions.

Via Christophe Jacquet, Francis Martin
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Intracellular Action of a Secreted Peptide Required for Fungal Virulence

Intracellular Action of a Secreted Peptide Required for Fungal Virulence | microbial pathogenesis and plant immunity | Scoop.it
Highlights 
• Qsp1 is an autoregulatory signaling peptide required for fungal virulence 
• Qsp1 controls intracellular growth, cell wall, and protease activities 
• Opt1 is a peptide transporter required for Qsp1 action in receiving cells 
• Intracellular expression of mature Qsp1 complements qsp1Δ phenotypes 

Summary 
Quorum sensing (QS) is a bacterial communication mechanism in which secreted signaling molecules impact population function and gene expression. QS-like phenomena have been reported in eukaryotes with largely unknown contributing molecules, functions, and mechanisms. We identify Qsp1, a secreted peptide, as a central signaling molecule that regulates virulence in the fungal pathogen Cryptococcus neoformans. QSP1 is a direct target of three transcription factors required for virulence, and qsp1Δ mutants exhibit attenuated infection, slowed tissue accumulation, and greater control by primary macrophages. Qsp1 mediates autoregulatory signaling that modulates secreted protease activity and promotes cell wall function at high cell densities. Peptide production requires release from a secreted precursor, proQsp1, by a cell-associated protease, Pqp1. Qsp1 sensing requires an oligopeptide transporter, Opt1, and remarkably, cytoplasmic expression of mature Qsp1 complements multiple phenotypes of qsp1Δ. Thus, C. neoformans produces an autoregulatory peptide that matures extracellularly but functions intracellularly to regulate virulence.

Via IPM Lab, Steve Marek
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Nature Microbiology: A fungal pathogen secretes plant alkalinizing peptides to increase
infection (2016)

Nature Microbiology: A fungal pathogen secretes plant alkalinizing peptides to increase<br/>                    infection (2016) | microbial pathogenesis and plant immunity | Scoop.it

Plant infections caused by fungi are often associated with an increase in the pH of the surrounding host tissue1. Extracellular alkalinization is thought to contribute to fungal pathogenesis, but the underlying mechanisms are poorly understood. Here, we show that the root-infecting fungus Fusarium oxysporum uses a functional homologue of the plant regulatory peptide RALF (rapid alkalinization factor)2,3 to induce alkalinization and cause disease in plants. An upshift in extracellular pH promotes infectious growth of Fusarium by stimulating phosphorylation of a conserved mitogen-activated protein kinase essential for pathogenicity4,5. Fungal mutants lacking a functional Fusarium (F)-RALF peptide failed to induce host alkalinization and showed markedly reduced virulence in tomato plants, while eliciting a strong host immune response. Arabidopsis plants lacking the receptor-like kinase FERONIA, which mediates the RALF-triggered alkalinization response6, displayed enhanced resistance against Fusarium. RALF homologues are found across a number of phylogenetically distant groups of fungi, many of which infect plants. We propose that fungal pathogens use functional homologues of alkalinizing peptides found in their host plants to increase their infectious potential and suppress host immunity.


Via Kamoun Lab @ TSL
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Mol Plant Pathol: Bacterial pathogenesis of plants: Future challenges from a microbial perspective (2016)

Mol Plant Pathol: Bacterial pathogenesis of plants: Future challenges from a microbial perspective (2016) | microbial pathogenesis and plant immunity | Scoop.it
Plant infection is a complicated process. Upon encountering a plant, pathogenic microorganisms must first adapt to life on the epiphytic surface, and survive long enough to initiate an infection. Responsiveness to the environment is critical throughout infection, with intracellular and community-level signal transduction pathways integrating environmental signals and triggering appropriate responses in the bacterial population. Ultimately, phytopathogens must migrate from the epiphytic surface into the plant tissue using motility and chemotaxis pathways. This migration is coupled to overcoming the physical and chemical barriers to entry into the plant apoplast. Once inside the plant, bacteria use an array of secretion systems to release phytotoxins and protein effectors that fulfil diverse pathogenic functions (Fig. 1)(Phan Tran et al., 2011, Melotto & Kunkel, 2013).

Via The Sainsbury Lab, Ronny Kellner, Kamoun Lab @ TSL
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The Sainsbury Lab's curator insight, May 16, 4:03 AM
Plant infection is a complicated process. Upon encountering a plant, pathogenic microorganisms must first adapt to life on the epiphytic surface, and survive long enough to initiate an infection. Responsiveness to the environment is critical throughout infection, with intracellular and community-level signal transduction pathways integrating environmental signals and triggering appropriate responses in the bacterial population. Ultimately, phytopathogens must migrate from the epiphytic surface into the plant tissue using motility and chemotaxis pathways. This migration is coupled to overcoming the physical and chemical barriers to entry into the plant apoplast. Once inside the plant, bacteria use an array of secretion systems to release phytotoxins and protein effectors that fulfil diverse pathogenic functions (Fig. 1)(Phan Tran et al., 2011, Melotto & Kunkel, 2013).
The Pub Club's curator insight, May 17, 8:23 AM
recommended by our friends at The Sainsbury Laboratory
Rakesh Yashroy's curator insight, May 18, 9:54 PM
Host-pathogen interface is the real battle field of survival against odds both for animals and plant infections @ https://en.wikipedia.org/wiki/Host-pathogen_interface
Rescooped by Jim Alfano from Plants and Microbes
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Nature Biotech: Accelerated cloning of a potato late blight–resistance gene using RenSeq and SMRT sequencing (2016)

Nature Biotech: Accelerated cloning of a potato late blight–resistance gene using RenSeq and SMRT sequencing (2016) | microbial pathogenesis and plant immunity | Scoop.it

Global yields of potato and tomato crops have fallen owing to potato late blight disease, which is caused by Phytophthora infestans. Although most commercial potato varieties are susceptible to blight, many wild potato relatives show variation for resistance and are therefore a potential source of Resistance to P. infestans (Rpi) genes. Resistance breeding has exploited Rpi genes from closely related tuber-bearing potato relatives, but is laborious and slow1, 2, 3. Here we report that the wild, diploid non-tuber-bearing Solanum americanum harbors multiple Rpi genes. We combine resistance (R) gene sequence capture (RenSeq)4 with single-molecule real-time (SMRT) sequencing (SMRT RenSeq) to clone Rpi-amr3i. This technology should enable de novo assembly of complete nucleotide-binding, leucine-rich repeat receptor (NLR) genes, their regulatory elements and complex multi-NLR loci from uncharacterized germplasm. SMRT RenSeq can be applied to rapidly clone multiple R genes for engineering pathogen-resistant crops.


Via The Sainsbury Lab, Kamoun Lab @ TSL
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The Sainsbury Lab's curator insight, April 26, 4:21 AM
Global yields of potato and tomato crops have fallen owing to potato late blight disease, which is caused by Phytophthora infestans. Although most commercial potato varieties are susceptible to blight, many wild potato relatives show variation for resistance and are therefore a potential source of Resistance to P. infestans (Rpi) genes. Resistance breeding has exploited Rpi genes from closely related tuber-bearing potato relatives, but is laborious and slow1, 2, 3. Here we report that the wild, diploid non-tuber-bearing Solanum americanum harbors multiple Rpi genes. We combine resistance (R) gene sequence capture (RenSeq)4 with single-molecule real-time (SMRT) sequencing (SMRT RenSeq) to clone Rpi-amr3i. This technology should enable de novo assembly of complete nucleotide-binding, leucine-rich repeat receptor (NLR) genes, their regulatory elements and complex multi-NLR loci from uncharacterized germplasm. SMRT RenSeq can be applied to rapidly clone multiple R genes for engineering pathogen-resistant crops.
Rescooped by Jim Alfano from Plant pathogens and pests
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mBio: Ralstonia solanacearum Type III Effector RipAY Is a Glutathione-Degrading Enzyme That Is Activated by Plant Cytosolic Thioredoxins and Suppresses Plant Immunity

mBio: Ralstonia solanacearum Type III Effector RipAY Is a Glutathione-Degrading Enzyme That Is Activated by Plant Cytosolic Thioredoxins and Suppresses Plant Immunity | microbial pathogenesis and plant immunity | Scoop.it
The plant pathogen Ralstonia solanacearum uses a large repertoire of type III effector proteins to succeed in infection. To clarify the function of effector proteins in host eukaryote cells, we expressed effectors in yeast cells and identified seven effector proteins that interfere with yeast growth. One of the effector proteins, RipAY, was found to share homology with the ChaC family proteins that function as γ-glutamyl cyclotransferases, which degrade glutathione (GSH), a tripeptide that plays important roles in the plant immune system. RipAY significantly inhibited yeast growth and simultaneously induced rapid GSH depletion when expressed in yeast cells. The in vitro GSH degradation activity of RipAY is specifically activated by eukaryotic factors in the yeast and plant extracts. Biochemical purification of the yeast protein identified that RipAY is activated by thioredoxin TRX2. On the other hand, RipAY was not activated by bacterial thioredoxins. Interestingly, RipAY was activated by plant h-type thioredoxins that exist in large amounts in the plant cytosol, but not by chloroplastic m-, f-, x-, y- and z-type thioredoxins, in a thiol-independent manner. The transient expression of RipAY decreased the GSH level in plant cells and affected the flg22-triggered production of reactive oxygen species (ROS) and expression of pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) marker genes in Nicotiana benthamiana leaves. These results indicate that RipAY is activated by host cytosolic thioredoxins and degrades GSH specifically in plant cells to suppress plant immunity.

Via Christophe Jacquet
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eLIFE: Arabidopsis heterotrimeric G proteins regulate immunity by directly coupling to the FLS2 receptor

eLIFE: Arabidopsis heterotrimeric G proteins regulate immunity by directly coupling to the FLS2 receptor | microbial pathogenesis and plant immunity | Scoop.it
The Arabidopsis immune receptor FLS2 perceives bacterial flagellin epitope flg22 to activate defenses through the central cytoplasmic kinase BIK1. The heterotrimeric G proteins composed of the non-canonical Gα protein XLG2, the Gβ protein AGB1, and the Gγ proteins AGG1 and AGG2 are required for FLS2-mediated immune responses through an unknown mechanism. Here we show that in the pre-activation state, XLG2 directly interacts with FLS2 and BIK1, and it functions together with AGB1 and AGG1/2 to attenuate proteasome-mediated degradation of BIK1, allowing optimum immune activation. Following the activation by flg22, XLG2 dissociates from AGB1 and is phosphorylated by BIK1 in the N terminus. The phosphorylated XLG2 enhances the production of reactive oxygen species (ROS) likely by modulating the NADPH oxidase RbohD. The study demonstrates that the G proteins are directly coupled to the FLS2 receptor complex and regulate immune signaling through both pre-activation and post-activation mechanisms.

Via Christophe Jacquet, Suayib Üstün
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PLOS Pathog: The E3 Ligase APIP10 Connects the Effector AvrPiz-t to the NLR Receptor Piz-t in Rice

PLOS Pathog: The E3 Ligase APIP10 Connects the Effector AvrPiz-t to the NLR Receptor Piz-t in Rice | microbial pathogenesis and plant immunity | Scoop.it
Although nucleotide-binding domain, leucine-rich repeat (NLR) proteins are the major immune receptors in plants, the mechanism that controls their activation and immune signaling remains elusive. Here, we report that the avirulence effector AvrPiz-t from Magnaporthe oryzae targets the rice E3 ligase APIP10 for degradation, but that APIP10, in return, ubiquitinates AvrPiz-t and thereby causes its degradation. Silencing of APIP10 in the non-Piz-t background compromises the basal defense against M. oryzae. Conversely, silencing of APIP10 in the Piz-t background causes cell death, significant accumulation of Piz-t, and enhanced resistance to M. oryzae, suggesting that APIP10 is a negative regulator of Piz-t. We show that APIP10 promotes degradation of Piz-t via the 26S proteasome system. Furthermore, we demonstrate that AvrPiz-t stabilizes Piz-t during M. oryzae infection. Together, our results show that APIP10 is a novel E3 ligase that functionally connects the fungal effector AvrPiz-t to its NLR receptor Piz-t in rice.

Via Suayib Üstün, Tatsuya Nobori
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Curr Opinion Plant Biol: Long-distance transport of phytohormones through the plant vascular system

Curr Opinion Plant Biol: Long-distance transport of phytohormones through the plant vascular system | microbial pathogenesis and plant immunity | Scoop.it
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Via Tatsuya Nobori
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Cellular Microbiology: Arabidopsis late blight: Infection of a nonhost plant by Albugo laibachii enables full colonization by Phytophthora infestans (2016)

Cellular Microbiology: Arabidopsis late blight: Infection of a nonhost plant by Albugo laibachii enables full colonization by Phytophthora infestans (2016) | microbial pathogenesis and plant immunity | Scoop.it

The oomycete pathogen Phytophthora infestans causes potato late blight, and as a potato and tomato specialist pathogen, is seemingly poorly adapted to infect plants outside the Solanaceae. Here, we report the unexpected finding that P. infestans can infect Arabidopsis thaliana when another oomycete pathogen, Albugo laibachii, has colonized the host plant. The behaviour and speed of P. infestans infection in Arabidopsis pre-infected with A. laibachii resemble P. infestans infection of susceptible potato plants. Transcriptional profiling of P. infestans genes during infection revealed a significant overlap in the sets of secreted-protein genes that are induced in P. infestans upon colonization of potato and susceptible Arabidopsis, suggesting major similarities in P. infestans gene expression dynamics on the two plant species. Furthermore, we found haustoria of A. laibachii and P. infestans within the same Arabidopsis cells. This Arabidopsis - A. laibachii - P. infestans tripartite interaction opens up various possibilities to dissect the molecular mechanisms of P. infestans infection and the processes occurring in co-infected Arabidopsis cells.


Via Kamoun Lab @ TSL
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The Arabidopsis Malectin-Like/LRR-RLK IOS1 is Critical for BAK1-Dependent and BAK1-Independent Pattern-Triggered Immunity

The Arabidopsis Malectin-Like/LRR-RLK IOS1 is Critical for BAK1-Dependent and BAK1-Independent Pattern-Triggered Immunity | microbial pathogenesis and plant immunity | Scoop.it
Plasma membrane-localized pattern recognition receptors (PRRs) such as FLAGELLIN SENSING2 (FLS2), EF-TU RECEPTOR (EFR) and CHITIN ELICITOR RECEPTOR KINASE 1 (CERK1) recognize microbe-associated molecular patterns (MAMPs) to activate pattern-triggered immunity (PTI). A reverse genetics approach on genes responsive to the priming agent beta-aminobutyric acid (BABA) revealed IMPAIRED OOMYCETE SUSCEPTIBILITY1 (IOS1) as a critical PTI player. Arabidopsis thaliana ios1 mutants were hyper-susceptible to Pseudomonas syringae bacteria. Accordingly, ios1 mutants showed defective PTI responses, notably delayed up-regulation of the PTI-marker gene FLG22-INDUCED RECEPTOR-LIKE KINASE1 (FRK1), reduced callose deposition and mitogen-activated protein kinase activation upon MAMP treatment. Moreover, Arabidopsis lines over-expressing IOS1 were more resistant to bacteria and showed a primed PTI response. In vitro pull-down, bimolecular fluorescence complementation, co-immunoprecipitation, and mass spectrometry analyses supported the existence of complexes between the membrane-localized IOS1 and BRASSINOSTEROID INSENSITIVE1-ASSOCIATED KINASE1 (BAK1)-dependent PRRs FLS2 and EFR, as well as with the BAK1-independent PRR CERK1. IOS1 also associated with BAK1 in a ligand-independent manner, and positively regulated FLS2-BAK1 complex formation upon MAMP treatment. In addition, IOS1 was critical for chitin-mediated PTI. Finally, ios1 mutants were defective in BABA-induced resistance and priming. This work reveals IOS1 as a novel regulatory protein of FLS2-, EFR- and CERK1-mediated signaling pathways that primes PTI activation.

Via Suayib Üstün, Tatsuya Nobori
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Plant Cell Physiol: Effector-triggered Immunity Determines Host Genotype-specific Incompatibility in Legume-Rhizobium Symbiosis

Symbiosis between legumes and rhizobia leads to the formation of N2-fixing root nodules. In soybean, several host genes, referred to as Rj genes, control nodulation. Soybean cultivars carrying Rj4 gene restrict nodulation by specific rhizobia such as Bradyrhizobium elkanii. We previously reported that the restriction of nodulation was caused by the B. elkanii possessing a functional type III secretion system (T3SS), which is known for its delivery of virulence factors by pathogenic bacteria. In the present study, we investigated the molecular basis for the T3SS-dependent nodulation restriction in Rj4-soybean. Inoculation tests revealed that soybean cultivar BARC-2 (Rj4/Rj4) restricted nodulation by B. elkanii USDA61, whereas its nearly isogenic line BARC-3 (rj4/rj4) formed nitrogen-fixing nodules with the same strain. Root-hair curling and infection thread were not observed in the roots of BARC-2 inoculated with USDA61, indicating that Rj4 blocked B. elkanii infection in the early stages. Accumulation of H2O2 and salicylic acid (SA) was observed in the roots of BARC-2 inoculated with USDA61. Transcriptome analyses revealed that inoculation of USDA61, but not its T3SS mutant in BARC-2 induced defense-related genes, including those coding for hypersensitive-induced responsive protein, which act in effector-triggered immunity (ETI) in Arabidopsis. These findings suggest that B. elkanii T3SS triggers SA-mediated ETI-type response in Rj4-soybean, which consequently blocks symbiotic interactions. This study revealed a common molecular mechanism underlying both plant–pathogen and plant–symbiont interactions and suggests that establishment of a root nodule symbiosis requires the evasion or suppression of plant immune responses triggered by rhizobial effectors.

Via Jean-Michel Ané
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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) | microbial pathogenesis and 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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Nature Microbiology: Fungal pathogenesis: Host modulation every which way (2016)

Nature Microbiology: Fungal pathogenesis: Host modulation every which way (2016) | microbial pathogenesis and plant immunity | Scoop.it

The plant pathogenic fungus Fusarium oxysporum secretes an effector that is similar to a plant peptide hormone, underscoring the variety of mechanisms that plant pathogens have evolved to tamper with host physiology.

 

Plant pathogens cause devastating diseases of crop plants and threaten food security in an era of continuous population growth. Annual losses due to fungal and oomycete diseases amount to enough food calories to feed at least half a billion people. Understanding how plant pathogens infect and colonize plants should help to develop disease-resistant crops. It appears that plant pathogens are sophisticated manipulators of their hosts. They secrete effector molecules that alter host biological processes in a variety of ways, generally promoting the pathogen lifestyle. A new study by Masachis, Segorbe and colleagues describes a new mechanism by which plant pathogens interfere with plant physiology. They discovered that the root-infecting fungus F. oxysporum secretes a peptide similar to the plant regulatory peptide RALF (rapid alkalinization factor) to induce host tissue alkalinization and enhance plant colonization. This study demonstrates that in addition to secreting classical plant hormones (or mimics thereof), fungi have also evolved functional homologues of plant peptides to alter host cellular processes.


Via Kamoun Lab @ TSL
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The Pseudomonas syringae type-III effector HopG1 induces actin remodeling to promote symptom development and susceptibility during infection

The plant cytoskeleton underpins the function of a multitude of cellular mechanisms, including those associated with developmental- and stress-associated signaling processes. In recent years, the actin cytoskeleton has been demonstrated to play a key role in plant immune signaling, including a recent demonstration that pathogens target actin filaments to block plant defense and immunity. Herein, we quantified spatial changes in host actin filament organization following infection with Pseudomonas syringae pv. tomato DC3000 (Pst DC3000), demonstrating that the type III effector HopG1 is required for pathogen-induced changes to actin filament architecture and host disease symptom development during infection. Using a suite of pathogen effector deletion constructs, coupled with high resolution microscopy, we found that deletion of hopG1 from Pst DC3000 resulted in a reduction in actin bundling, a concomitant increase in the density of filament arrays in Arabidopsis, both of which correlate with host disease symptom development. As a mechanism underpinning this activity, we further show that the HopG1 effector interacts with an Arabidopsis mitochondrial-localized kinesin motor protein. Kinesin mutant plants show reduced disease symptoms following pathogen infection, which can be complemented by actin modifying agents. In total, our results support a model in which HopG1 induces changes in the organization of the actin cytoskeleton as part of its virulence function in promoting disease symptom development.

Via Suayib Üstün
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PLOS Pathog: Direct and Indirect Targeting of PP2A by Conserved Bacterial Type-III Effector Proteins

PLOS Pathog: Direct and Indirect Targeting of PP2A by Conserved Bacterial Type-III Effector Proteins | microbial pathogenesis and plant immunity | Scoop.it
Bacterial AvrE-family Type-III effector proteins (T3Es) contribute significantly to the virulence of plant-pathogenic species of Pseudomonas, Pantoea, Ralstonia, Erwinia, Dickeya and Pectobacterium, with hosts ranging from monocots to dicots. However, the mode of action of AvrE-family T3Es remains enigmatic, due in large part to their toxicity when expressed in plant or yeast cells. To search for targets of WtsE, an AvrE-family T3E from the maize pathogen Pantoea stewartii subsp. stewartii, we employed a yeast-two-hybrid screen with non-lethal fragments of WtsE and a synthetic genetic array with full-length WtsE. Together these screens indicate that WtsE targets maize protein phosphatase 2A (PP2A) heterotrimeric enzyme complexes via direct interaction with B’ regulatory subunits. AvrE1, another AvrE-family T3E from Pseudomonas syringae pv. tomato strain DC3000 (Pto DC3000), associates with specific PP2A B’ subunit proteins from its susceptible host Arabidopsis that are homologous to the maize B’ subunits shown to interact with WtsE. Additionally, AvrE1 was observed to associate with the WtsE-interacting maize proteins, indicating that PP2A B’ subunits are likely conserved targets of AvrE-family T3Es. Notably, the ability of AvrE1 to promote bacterial growth and/or suppress callose deposition was compromised in Arabidopsis plants with mutations of PP2A genes. Also, chemical inhibition of PP2A activity blocked the virulence activity of both WtsE and AvrE1 in planta. The function of HopM1, a Pto DC3000 T3E that is functionally redundant to AvrE1, was also impaired in specific PP2A mutant lines, although no direct interaction with B’ subunits was observed. These results indicate that sub-component specific PP2A complexes are targeted by bacterial T3Es, including direct targeting by members of the widely conserved AvrE-family.

Via Suayib Üstün, Tatsuya Nobori
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fundoshi's curator insight, May 20, 6:17 AM
Hop好きだけど いよいよ応用には今後しばらく結びつかないのかなって感でてきた気がする
Rescooped by Jim Alfano from Plants and Microbes
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Nature Biotech: Rapid cloning of disease-resistance genes in plants using mutagenesis and sequence capture (2016)

Nature Biotech: Rapid cloning of disease-resistance genes in plants using mutagenesis and sequence capture (2016) | microbial pathogenesis and plant immunity | Scoop.it

Wild relatives of domesticated crop species harbor multiple, diverse, disease resistance (R) genes that could be used to engineer sustainable disease control. However, breeding R genes into crop lines often requires long breeding timelines of 5–15 years to break linkage between R genes and deleterious alleles (linkage drag). Further, when R genes are bred one at a time into crop lines, the protection that they confer is often overcome within a few seasons by pathogen evolution1. If several cloned R genes were available, it would be possible to pyramid R genes2 in a crop, which might provide more durable resistance1. We describe a three-step method (MutRenSeq)-that combines chemical mutagenesis with exome capture and sequencing for rapid R gene cloning. We applied MutRenSeq to clone stem rust resistance genes Sr22 and Sr45 from hexaploid bread wheat. MutRenSeq can be applied to other commercially relevant crops and their relatives, including, for example, pea, bean, barley, oat, rye, rice and maize.


Via The Sainsbury Lab, Kamoun Lab @ TSL
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The Sainsbury Lab's curator insight, April 26, 4:14 AM
Wild relatives of domesticated crop species harbor multiple, diverse, disease resistance (R) genes that could be used to engineer sustainable disease control. However, breeding R genes into crop lines often requires long breeding timelines of 5–15 years to break linkage between R genes and deleterious alleles (linkage drag). Further, when R genes are bred one at a time into crop lines, the protection that they confer is often overcome within a few seasons by pathogen evolution1. If several cloned R genes were available, it would be possible to pyramid R genes2 in a crop, which might provide more durable resistance1. We describe a three-step method (MutRenSeq)-that combines chemical mutagenesis with exome capture and sequencing for rapid R gene cloning. We applied MutRenSeq to clone stem rust resistance genes Sr22 and Sr45 from hexaploid bread wheat. MutRenSeq can be applied to other commercially relevant crops and their relatives, including, for example, pea, bean, barley, oat, rye, rice and maize.
Neelam Redekar's curator insight, April 29, 8:19 AM
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Rescooped by Jim Alfano from Plants and Microbes
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Nature Biotech: A pigeonpea gene confers resistance to Asian soybean rust in soybean (2016)

Nature Biotech: A pigeonpea gene confers resistance to Asian soybean rust in soybean (2016) | microbial pathogenesis and plant immunity | Scoop.it

Asian soybean rust (ASR), caused by the fungus Phakopsora pachyrhizi, is one of the most economically important crop diseases, but is only treatable with fungicides, which are becoming less effective owing to the emergence of fungicide resistance. There are no commercial soybean cultivars with durable resistance to P. pachyrhizi, and although soybean resistance loci have been mapped, no resistance genes have been cloned. We report the cloning of a P. pachyrhizi resistance gene CcRpp1 (Cajanus cajan Resistance against Phakopsora pachyrhizi 1) from pigeonpea (Cajanus cajan) and show that CcRpp1 confers full resistance to P. pachyrhizi in soybean. Our findings show that legume species related to soybean such as pigeonpea, cowpea, common bean and others could provide a valuable and diverse pool of resistance traits for crop improvement.


Via The Sainsbury Lab, Kamoun Lab @ TSL
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The Sainsbury Lab's curator insight, April 26, 4:45 AM
Asian soybean rust (ASR), caused by the fungus Phakopsora pachyrhizi, is one of the most economically important crop diseases, but is only treatable with fungicides, which are becoming less effective owing to the emergence of fungicide resistance. There are no commercial soybean cultivars with durable resistance to P. pachyrhizi, and although soybean resistance loci have been mapped, no resistance genes have been cloned. We report the cloning of a P. pachyrhizi resistance gene CcRpp1 (Cajanus cajan Resistance against Phakopsora pachyrhizi 1) from pigeonpea (Cajanus cajan) and show that CcRpp1 confers full resistance to P. pachyrhizi in soybean. Our findings show that legume species related to soybean such as pigeonpea, cowpea, common bean and others could provide a valuable and diverse pool of resistance traits for crop improvement.
Rescooped by Jim Alfano from Plant-microbe interaction
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Decoy engineering: the next step in resistance breeding: Trends in Plant Science

Decoy engineering: the next step in resistance breeding: Trends in Plant Science | microbial pathogenesis and plant immunity | Scoop.it

.Until recently it was not possible to engineer novel recognition specificities of classical plant immune receptors to completely unrelated effectors. In a recent publication, Kim et al. engineered a plant effector target to increase novel recognition specificities by trapping unrelated pathogen-derived proteases in their act [1].

RESISTANCE TO PSEUDOMONAS SYRINGAE 5 (RPS5) is a plant immune receptor of the Nucleotide-binding, leucine-rich repeat (NLR) type which perceives the Pseudomonas syringae Type-III effector AvrPphB, a papain-like cysteine protease belonging to the Peptidase C58 family [2]. The perception of AvrPphB by RPS5 requires one additional host-derived factor known as AVRPPHB SUSCEPTIBLE 1 (PBS1), which belongs to Subfamily VII of Receptor-like Cytoplasmic Kinases (RLCK VII). Upon bacterial infection, PBS1, which binds to RPS5 in its pre-activation state, is cleaved by AvrPphB. PBS1 cleavage exposes a five amino acid loop in PBS1 that is believed to activate RPS5, triggering an immune response characterized by the hypersensitive response (HR), a form of programmed cell death [3]. Interestingly, RPS5-mediated immune signaling requires both PBS1 fragments, and the conformational change induced by cleavage can be mimicked by insertion of five amino acids in the AvrPphB cleavage site [4]. Therefore, perception of AvrPphB follows a mouse-trap mechanism where cleavage of PBS1 (bait) sets off the trap and activates RPS5, triggering immune responses..


Via Christophe Jacquet, Suayib Üstün
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Nat Commun: A Phytophthora infestans RXLR effector targets plant PP1c isoforms that promote late blight disease (2016)

Nat Commun: A Phytophthora infestans RXLR effector targets plant PP1c isoforms that promote late blight disease (2016) | microbial pathogenesis and plant immunity | Scoop.it

Plant pathogens deliver effectors to alter host processes. Knowledge of how effectors target and manipulate host proteins is critical to understand crop disease. Here, we show that in plantaexpression of the RXLR effector Pi04314 enhances leaf colonization by Phytophthora infestans via activity in the host nucleus and attenuates induction of jasmonic and salicylic acid-responsive genes. Pi04314 interacts with three host protein phosphatase 1 catalytic (PP1c) isoforms, causing their re-localization from the nucleolus to the nucleoplasm. Re-localization of PP1c-1 also occurs during infection and is dependent on an R/KVxF motif in the effector. Silencing the PP1c isoforms or overexpression of a phosphatase-dead PP1c-1 mutant attenuates infection, demonstrating that host PP1c activity is required for disease. Moreover, expression of PP1c–1mut abolishes enhanced leaf colonization mediated by in planta Pi04314 expression. We argue that PP1c isoforms are susceptibility factors forming holoenzymes with Pi04314 to promote late blight disease.


Via Kamoun Lab @ TSL
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