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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) | Plants and Microbes | 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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Plant Cell: Interaction of the Arabidopsis GTPase RabA4c with Its Effector PMR4 Results in Complete Penetration Resistance to Powdery Mildew (2014)

Plant Cell: Interaction of the Arabidopsis GTPase RabA4c with Its Effector PMR4 Results in Complete Penetration Resistance to Powdery Mildew (2014) | Plants and Microbes | Scoop.it

The (1,3)-β-glucan callose is a major component of cell wall thickenings in response to pathogen attack in plants. GTPases have been suggested to regulate pathogen-induced callose biosynthesis. To elucidate the regulation of callose biosynthesis in Arabidopsis thaliana, we screened microarray data and identified transcriptional upregulation of the GTPase RabA4c after biotic stress. We studied the function of RabA4c in its native and dominant negative (dn) isoform inRabA4c overexpression lines. RabA4c overexpression caused complete penetration resistance to the virulent powdery mildew Golovinomyces cichoracearum due to enhanced callose deposition at early time points of infection, which prevented fungal ingress into epidermal cells. By contrast,RabA4c(dn) overexpression did not increase callose deposition or penetration resistance. A cross of the resistant line with the pmr4 disruption mutant lacking the stress-induced callose synthase PMR4 revealed that enhanced callose deposition and penetration resistance were PMR4-dependent. In live-cell imaging, tagged RabA4c was shown to localize at the plasma membrane prior to infection, which was broken in the pmr4 disruption mutant background, with callose deposits at the site of attempted fungal penetration. Together with our interactions studies including yeast two-hybrid, pull-down, and in planta fluorescence resonance energy transfer assays, we concluded that RabA4c directly interacts with PMR4, which can be seen as an effector of this GTPase.

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PLOS Pathogens: Pto Kinase Binds Two Domains of AvrPtoB and Its Proximity to the Effector E3 Ligase Determines if It Evades Degradation and Activates Plant Immunity (2014)

PLOS Pathogens: Pto Kinase Binds Two Domains of AvrPtoB and Its Proximity to the Effector E3 Ligase Determines if It Evades Degradation and Activates Plant Immunity (2014) | Plants and Microbes | Scoop.it

The tomato—Pseudomonas syringae pv. tomato (Pst)—pathosystem is one of the best understood models for plant-pathogen interactions. Certain wild relatives of tomato express two closely related members of the same kinase family, Pto and Fen, which recognize the Pstvirulence protein AvrPtoB and activate effector-triggered immunity (ETI). AvrPtoB, however, contains an E3 ubiquitin ligase domain in its carboxyl terminus which causes degradation of Fen and undermines its ability to activate ETI. In contrast, Pto evades AvrPtoB-mediated degradation and triggers ETI in response to the effector. It has been reported recently that Pto has higher kinase activity than Fen and that this difference allows Pto to inactivate the E3 ligase through phosphorylation of threonine-450 (T450) in AvrPtoB. Here we show that, in contrast to Fen which can only interact with a single domain proximal to the E3 ligase of AvrPtoB, Pto binds two distinct domains of the effector, the same site as Fen and another N-terminal domain. In the absence of E3 ligase activity Pto binds to either domain of AvrPtoB to activate ETI. However, the presence of an active E3 ligase domain causes ubiquitination of Pto that interacts with the domain proximal to the E3 ligase, identical to ubiquitination of Fen. Only when Pto binds its unique distal domain can it resist AvrPtoB-mediated degradation and activate ETI. We show that phosphorylation of T450 is not required for Pto-mediated resistance in vivo and that a kinase-inactive version of Pto is still capable of activating ETI in response to AvrPtoB. Our results demonstrate that the ability of Pto to interact with a second site distal to the E3 ligase domain in AvrPtoB, and not a higher kinase activity or T450 phosphorylation, allows Pto to evade ubiquitination and to confer immunity to Pst.

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Mashable: Chinese Researchers Create Disease-Resistant Wheat by Deleting Genes (2014)

Mashable: Chinese Researchers Create Disease-Resistant Wheat by Deleting Genes (2014) | Plants and Microbes | Scoop.it

Advanced genome-editing techniques have been used to create a strain of wheat resistant to a destructive fungal pathogen — called powdery mildew — that is a major bane to the world's top food source, according to scientists at one of China's leading centers for agricultural research.


To stop the mildew, researchers at the Chinese Academy of Sciences deleted genes that encode proteins that repress defenses against the mildew. The work promises to someday make wheat more resistant to the disease, which is typically controlled through the heavy use of fungicides. It also represents an important achievement in using genome editing tools to engineer food crops without inserting foreign genes — a flashpoint for opposition to genetically modified crops.


The gene-deletion trick is particularly tough to do in wheat because the plant has three genomes — with largely similar copies of the same genes — meaning all three must be deleted or the trait will not be changed. Using gene-editing tools known as TALENs and CRISPR, the researchers were able to do that without changing anything else or adding genes from other organisms.


"We now caught all three copies, and only by knocking out all three copies can we get this [mildew]-resistant phenotype," says Caixia Gao, who heads a gene-editing research group at the State Key Laboratory of Plant Cell and Chromosome Engineering at the Institute of Microbiology in Beijing.


A paper describing the results appears in Nature Biotechnology http://dx.doi.org/10.1038/nbt.2969.

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MPMI: Comparative and functional analysis of the widely occurring family of Nep1-like proteins (2014)

MPMI: Comparative and functional analysis of the widely occurring family of Nep1-like proteins (2014) | Plants and Microbes | Scoop.it

Nep-1 Like Proteins (NLPs) are best known for their cytotoxic activity in dicot plants. NLPs are taxonomically widespread among microbes with very different lifestyles. To learn more about this enigmatic protein family we analyzed more than 500 available NLP protein sequences from fungi, oomycetes, and bacteria. Phylogenetic clustering showed that, besides the previously documented two types, an additional more divergent third NLP type could be distinguished. By closely examining the three NLP types, we identified a non-cytotoxic subgroup of type 1 NLPs (designated type 1a), which have substitutions in amino acids making up a cation-binding pocket that is required for cytotoxicity. Type 2 NLPs were found to contain a putative calcium-binding motif, which was shown to be required for cytotoxicity. Members of both type 1 and type 2 NLPs were found to possess additional cysteine residues that, based on their predicted proximity, make up potential disulfide bridges that could provide additional stability to these secreted proteins. Type 1 and type 2 NLPs, although both cytotoxic to plant cells, differ in their ability to induce necrosis when artificially targeted to different cellular compartments in planta, suggesting they have different mechanisms of cytotoxicity.

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PLOS Pathog: An Immunity-Triggering Effector from the Barley Smut Fungus Ustilago hordei Resides in an Ustilaginaceae-Specific Cluster Bearing Signs of Transposable Element-Assisted Evolution (2014)

PLOS Pathog: An Immunity-Triggering Effector from the Barley Smut Fungus Ustilago hordei Resides in an Ustilaginaceae-Specific Cluster Bearing Signs of Transposable Element-Assisted Evolution (2014) | Plants and Microbes | Scoop.it

The basidiomycete smut fungus Ustilago hordei was previously shown to comprise isolates that are avirulent on various barley host cultivars. Through genetic crosses we had revealed that a dominant avirulence locus UhAvr1 which triggers immunity in barley cultivar Hannchen harboring resistance gene Ruh1, resided within an 80-kb region. DNA sequence analysis of this genetically delimited region uncovered the presence of 7 candidate secreted effector proteins. Sequence comparison of their coding sequences among virulent and avirulent parental and field isolates could not distinguish UhAvr1 candidates. Systematic deletion and complementation analyses revealed that UhAvr1 is UHOR_10022 which codes for a small effector protein of 171 amino acids with a predicted 19 amino acid signal peptide. Virulence in the parental isolate is caused by the insertion of a fragment of 5.5 kb with similarity to a common U. hordei transposable element (TE), interrupting the promoter of UhAvr1 and thereby changing expression and hence recognition of UhAVR1p. This rearrangement is likely caused by activities of TEs and variation is seen among isolates. Using GFP-chimeric constructs we show that UhAvr1 is induced only in mated dikaryotic hyphae upon sensing and infecting barley coleoptile cells. When infecting Hannchen, UhAVR1p causes local callose deposition and the production of reactive oxygen species and necrosis indicative of the immune response. UhAvr1 does not contribute significantly to overall virulence. UhAvr1 is located in a cluster of ten effectors with several paralogs and over 50% of TEs. This cluster is syntenous with clusters in closely-related U. maydis and Sporisorium reilianum. In these corn-infecting species, these clusters harbor however more and further diversified homologous effector families but very few TEs. This increased variability may have resulted from past selection pressure by resistance genes since U. maydis is not known to trigger immunity in its corn host.

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Annual Review of Phytopathology: Susceptibility Genes 101: How to Be a Good Host (2014)

Annual Review of Phytopathology: Susceptibility Genes 101: How to Be a Good Host (2014) | Plants and Microbes | Scoop.it

To confer resistance against pathogens and pests in plants, typically dominant resistance genes are deployed. However, because resistance is based on recognition of a single pathogen-derived molecular pattern these narrowspectrum genes are usually readily overcome. Disease arises from a compatible interaction between plant and pathogen. Hence, altering a plant gene that critically facilitates compatibility could provide a more broad-spectrum and durable type of resistance. Here, such susceptibility (S) genes are reviewed with a focus on the mechanisms underlying loss of compatibility. We distinguish three groups of S genes acting during different stages of infection: early pathogen establishment, modulation of host defenses, and pathogen sustenance. The many examples reviewed here show that S genes have the potential to be used in resistance breeding. However, because S genes have a function other than being a compatibility factor for the pathogen, the side effects caused by their mutation demands a one-by-one assessment of their usefulness for application.

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Cell Host & Microbe: Agrobacterium tumefaciens Deploys a Superfamily of Type VI Secretion DNase Effectors as Weapons for Interbacterial Competition In Planta (2014)

Cell Host & Microbe: Agrobacterium tumefaciens Deploys a Superfamily of Type VI Secretion DNase Effectors as Weapons for Interbacterial Competition In Planta (2014) | Plants and Microbes | Scoop.it

The type VI secretion system (T6SS) is a widespread molecular weapon deployed by many Proteobacteria to target effectors/toxins into both eukaryotic and prokaryotic cells. We report that Agrobacterium tumefaciens, a soil bacterium that triggers tumorigenesis in plants, produces a family of type VI DNase effectors (Tde) that are distinct from previously known polymorphic toxins and nucleases. Tde exhibits an antibacterial DNase activity that relies on a conserved HxxD motif and can be counteracted by a cognate immunity protein, Tdi. In vitro, A. tumefaciens T6SS could kill Escherichia coli but triggered a lethal counterattack by Pseudomonas aeruginosa upon injection of the Tde toxins. However, in an in planta coinfection assay, A. tumefaciens used Tde effectors to attack both siblings cells and P. aeruginosa to ultimately gain a competitive advantage. Such acquired T6SS-dependent fitness in vivo and conservation of Tde-Tdi couples in bacteria highlights a widespread antibacterial weapon beneficial for niche colonization


Via Suayib Üstün, Jim Alfano
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Storify: #MPMI2014 Day 4 of XVI IC-MPMI, Rhodes, Greece, 6-10 July

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Storify Tweet Archive of #MPMI2014 Days 1 and 2 of XVI IC-MPMI, Rhodes, Greece, 6-10 July

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Plant Physiology Cover — July 2014

Plant Physiology Cover  — July 2014 | Plants and Microbes | Scoop.it

Filamentous plant pathogens such as the late blight pathogenPhytophthora infestans form digit-like infection structures called haustoria inside plant cells. Haustoria enable the pathogen to feed on its host, and secrete effector proteins that modulate the physiology of the host cell to facilitate infection. Haustoria are enveloped by a specialized plant-derived membrane (the extrahaustorial membrane) the biogenesis of which is poorly understood. In this issue, Bozkurt et al. http://www.plantphysiol.org/content/165/3/1005 used the plant membrane microdomain protein REMORIN1.3, known to accumulate around P. infestans haustoria, to reveal discrete extrahaustorial domains labeled by REMORIN1.3 and P. infestans effector AVRblb2. SYNAPTOTAGMIN1, another previously identified perihaustorial protein, localized to subdomains which are mainly not labeled by REMORIN1.3 and AVRblb2. Functional characterization of REMORIN1.3 revealed that it is a susceptibility factor that promotes infection by P. infestans. This activity, and REMORIN1.3 recruitment to the EHM, require REM1.3 membrane-binding domain. These results implicate REMORIN1.3 membrane microdomains in plant susceptibility to an oomycete pathogen. The cover shows Nicotiana benthamiana epidermal cells expressing fluorescently labeled REMORIN1.3 (blue) infected by P. infestans expressing the red fluorescent protein (red). Cover image credits: Sylvain Raffaele.

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Plant J: Suppression among alleles encoding NB-LRR resistance proteins interferes with resistance in F1 hybrid and allele-pyramided wheat plants (2014)

Plant J: Suppression among alleles encoding NB-LRR resistance proteins interferes with resistance in F1 hybrid and allele-pyramided wheat plants (2014) | Plants and Microbes | Scoop.it

Developing high yielding varieties with broad-spectrum and durable disease resistance is the ultimate goal of crop breeding. In plants, immune receptors of the NB-LRR class mediate race-specific resistance against pathogen attack. This type of resistance is often rapidly overcome by newly adapted pathogen races when employed in agriculture. The stacking of different resistance genes or alleles in F1 hybrids or in pyramided lines is a promising strategy to achieve more durable resistance. Here, we identify a molecular mechanism which can negatively interfere with the allele-pyramiding approach. We show that pairwise combinations of different alleles of the powdery-mildew-resistance gene Pm3 in F1 hybrids and stacked transgenic wheat lines can result in suppression of Pm3-based resistance. This effect is independent of the genetic background and solely dependent on the Pm3 alleles. Suppression occurs at the post-translational level as neither RNA nor protein levels of the suppressed alleles are affected. Using a transient-expression system in Nicotiana benthamiana, the LRR domain was identified as the suppression-conferring domain. The results of this study suggest that the expression of closely related NB-LRR resistance genes or alleles in the same genotype can lead to dominant-negative interactions. These findings provide a molecular explanation for the frequently observed ineffectiveness of resistance genes introduced from the secondary gene pool into polyploid crop species and mark an important step to overcome this limitation.

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Plant & Cell Physiol: Ectopic Expression of RESISTANCE TO POWDERY MILDEW8.1 Confers Resistance to Fungal and Oomycete Pathogens in Arabidopsis (2014)

Plant & Cell Physiol: Ectopic Expression of RESISTANCE TO POWDERY MILDEW8.1 Confers Resistance to Fungal and Oomycete Pathogens in Arabidopsis (2014) | Plants and Microbes | Scoop.it

Broad-spectrum disease resistance is a highly valuable trait in plant breeding and attracts special attention in research. The Arabidopsis gene locus RESISTANCE TO POWDERY MILDEW 8 (RPW8) contains two adjacent homologous genes, RPW8.1 and RPW8.2, and confers broad-spectrum resistance to powdery mildew. Remarkably, the RPW8.2 protein is specifically localized to the extrahaustorial membrane (EHM) encasing the feeding structure of powdery mildew whereby RPW8.2 activates haustorium-targeted defenses. Here, we show that ectopic expression of the yellow fluorescent protein (YFP)-tagged RPW8.1 from the native promoter leads to unique cell death lesions and enhances resistance to virulent fungal and oomycete pathogens that cause powdery mildew and downy mildew diseases, respectively. In powdery mildew infected plants, RPW8.1-YFP accumulates at higher levels in the mesophyll cells underneath the infected epidermal cells where RPW8.2-YFP is mainly expressed. This cell-type-preferential protein accumulation pattern largely correlates with that of H2O2 accumulation, suggesting that RPW8.1 may spatially collaborate with RPW8.2 in activation of resistance to powdery mildew. Interestingly, when ectopically expressed from theRPW8.2 promoter, RPW8.1-YFP is also targeted to the EHM of powdery mildew and the transgenic plants display resistance to both powdery mildew and downy mildew. Using YFP as a reporter, we further reveal that the RPW8.1 promoter is constitutively active but induced to higher levels in cells at the infection site, whereas the RPW8.2 promoter is activated specifically in cells at the infection site. Taken together, our results suggest that RPW8.1 (and its promoter) is functionally distinct fromRPW8.2 and may have a higher potential in engineering broad-spectrum resistance in plants.

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Schornack Lab: a bursting spore of the arbuscular mycorrhiza fungus Rhizophagus irregularis - releasing oil droplets (2014)

Schornack Lab: a bursting spore of the arbuscular mycorrhiza fungus Rhizophagus irregularis - releasing oil droplets (2014) | Plants and Microbes | Scoop.it

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New Phytologist: Hitchhiker's guide to multi-dimensional plant pathology (2014)

New Phytologist: Hitchhiker's guide to multi-dimensional plant pathology (2014) | Plants and Microbes | Scoop.it

Filamentous pathogens pose a substantial threat to global food security. One central question in plant pathology is how pathogens cause infection and manage to evade or suppress plant immunity to promote disease. With many technological advances over the past decade, including DNA sequencing technology, an array of new tools has become embedded within the toolbox of next-generation plant pathologists. By employing a multidisciplinary approach plant pathologists can fully leverage these technical advances to answer key questions in plant pathology, aimed at achieving global food security. This review discusses the impact of: cell biology and genetics on progressing our understanding of infection structure formation on the leaf surface; biochemical and molecular analysis to study how pathogens subdue plant immunity and manipulate plant processes through effectors; genomics and DNA sequencing technologies on all areas of plant pathology; and new forms of collaboration on accelerating exploitation of big data. As we embark on the next phase in plant pathology, the integration of systems biology promises to provide a holistic perspective of plant–pathogen interactions from big data and only once we fully appreciate these complexities can we design truly sustainable solutions to preserve our resources.

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Nature: The long-term maintenance of a resistance polymorphism through diffuse interactions (2014)

Nature: The long-term maintenance of a resistance polymorphism through diffuse interactions (2014) | Plants and Microbes | Scoop.it

Plant resistance (R) genes are a crucial component in plant defence against pathogens1. Although R genes often fail to provide durable resistance in an agricultural context, they frequently persist as long-lived balanced polymorphisms in nature234. Standard theory explains the maintenance of such polymorphisms through a balance of the costs and benefits of resistance and virulence in a tightly coevolving host–pathogen pair56. However, many plant–pathogen interactions lack such specificity7. Whether, and how, balanced polymorphisms are maintained in diffusely interacting species8 is unknown. Here we identify a naturally interacting R gene and effector pair in Arabidopsis thaliana and its facultative plant pathogen, Pseudomonas syringae. The protein encoded by the R gene RPS5 recognizes an AvrPphB homologue (AvrPphB2) and exhibits a balanced polymorphism that has been maintained for over 2 million years (ref. 3). Consistent with the presence of an ancient balanced polymorphism, the R gene confers a benefit when plants are infected with P. syringae carrying avrPphB2 but also incurs a large cost in the absence of infection. RPS5alleles are maintained at intermediate frequencies in populations globally, suggesting ubiquitous selection for resistance. However, the presence of P. syringae carrying avrPphB is probably insufficient to explain the RPS5 polymorphism. First, avrPphB homologues occur at very low frequencies in P. syringae populations on A. thaliana. Second, AvrPphB only rarely confers a virulence benefit to P. syringae on A. thaliana. Instead, we find evidence that selection for RPS5 involves multiple non-homologous effectors and multiple pathogen species. These results and an associated model suggest that the R gene polymorphism in A. thaliana may not be maintained through a tightly coupled interaction involving a single coevolved R gene and effector pair. More likely, the stable polymorphism is maintained through complex and diffuse community-wide interactions.

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Nature Biotechnology: Simultaneous editing of three homoeoalleles in hexaploid bread wheat confers heritable resistance to powdery mildew (2014)

Nature Biotechnology: Simultaneous editing of three homoeoalleles in hexaploid bread wheat confers heritable resistance to powdery mildew (2014) | Plants and Microbes | Scoop.it

Sequence-specific nucleases have been applied toengineer targeted modifications in polyploid genomes, but simultaneous modification of multiple homoeoalleles has not been reported. Here we use transcription activator–like effector nuclease (TALEN) and clustered, regularly interspaced, short palindromic repeats (CRISPR)-Cas9 technologies in hexaploid bread wheat to introduce targeted mutations in the three homoeoalleles that encode MILDEW- RESISTANCE LOCUS (MLO) proteins. Genetic redundancy has prevented evaluation of whether mutation of all three MLO alleles in bread wheat might confer resistance to powdery mildew, a trait not found in natural populations. We show that TALEN-induced mutation of all three TaMLO homoeologs in the same plant confers heritable broad-spectrum resistanceto powdery mildew. We further use CRISPR-Cas9 technologyto generate transgenic wheat plants that carry mutations inthe TaMLO-A1 allele. We also demonstrate the feasibility of engineering targeted DNA insertion in bread wheat through nonhomologous end joining of the double-strand breaks caused by TALENs. Our findings provide a methodological framework to improve polyploid crops.



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Fesquet didier's curator insight, July 22, 2:22 AM

this open the way for developping non toxic wheat species...good for celiac people...maybe one day...hopes for a slice of pizza :-)

 

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ABC News: Canola virus wipes out crops in South Australia (2014)

ABC News: Canola virus wipes out crops in South Australia (2014) | Plants and Microbes | Scoop.it

Scientists say an outbreak of beet western yellows virus is one of the worst cases ever seen in Australia.


Early estimates suggest up to 10,000 hectares of canola have been affected, in South Australia's lower north, mid north and lower mallee regions. The virus is transported by green peach aphids, which have thrived in the state's recent warm and humid weather. Ag consultant Mick Faulkner says agronomists felt like they'd been "blind-sided" after not being able to work out what had been affecting crops. "It took everyone a fair bit of time to realise that we weren't killing the aphids," Mr Faulkner said. "Green paddocks are now brown. "Those that have been affected, I have grave fears that they won't yield anything at all."


Virus halted for now - The South Australian Research and Development Institute (SARDI) says it's now testing samples to confirm how the virus is spreading and where else it might turn up. Pulse pathologist Jenny Davidson says with cooler weather, the virus-transmitting aphids aren't moving and at the moment the best thing growers can do is "nothing", "We expect that the spread of this virus would've stopped for now, so there's no point people going out and spraying aphids now," she says. "It's also important growers ascertain it actually is the virus causing problems in their canola crops, there may be other things going on as well. "The potential risk is what these aphids will do in spring time. "We're not sure whether or not pulse crops are at risk but we'll have that information back well and truly before the spring time flights." Ms Davidson says the virus isn't uncommon, but what is unusual is the extent of damage and infection being seen. She says it's taken everyone by surprise. "I've never seen this level of damage from any virus in crops," Ms Davidson says. "It's the magnitude of what we're dealing with that is totally un-expected."

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EMBO J: The NB-LRR proteins RGA4 and RGA5 interact functionally and physically to confer disease resistance (2014)

EMBO J: The NB-LRR proteins RGA4 and RGA5 interact functionally and physically to confer disease resistance (2014) | Plants and Microbes | Scoop.it

Plant resistance proteins of the class of nucleotide-binding and leucine-rich repeat domain proteins (NB-LRRs) are immune sensors which recognize pathogen-derived molecules termed avirulence (AVR) proteins. We show that RGA4 and RGA5, two NB-LRRs from rice, interact functionally and physically to mediate resistance to the fungal pathogen Magnaporthe oryzae and accomplish different functions in AVR recognition. RGA4 triggers an AVR-independent cell death that is repressed in the presence of RGA5 in both rice protoplasts and Nicotiana benthamiana. Upon recognition of the pathogen effector AVR-Pia by direct binding to RGA5, repression is relieved and cell death occurs. RGA4 and RGA5 form homo- and hetero-complexes and interact through their coiled-coil domains. Localization studies in rice protoplast suggest that RGA4 and RGA5 localize to the cytosol. Upon recognition of AVR-Pia, neither RGA4 nor RGA5 is re-localized to the nucleus. These results establish a model for the interaction of hetero-pairs of NB-LRRs in plants: RGA4 mediates cell death activation, while RGA5 acts as a repressor of RGA4 and as an AVR receptor.

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New Phytologist: Gate control: guard cell regulation by microbial stress (2014)

New Phytologist: Gate control: guard cell regulation by microbial stress (2014) | Plants and Microbes | Scoop.it

Terrestrial plants rely on stomata, small pores in the leaf surface, for photosynthetic gas exchange and transpiration of water. The stomata, formed by a pair of guard cells, dynamically increase and decrease their volume to control the pore size in response to environmental cues. Stresses can trigger similar or opposing movements: for example, drought induces closure of stomata, whereas many pathogens exploit stomata and cause them to open to facilitate entry into plant tissues. The latter is an active process as stomatal closure is part of the plant's immune response. Stomatal research has contributed much to clarify the signalling pathways of abiotic stress, but guard cell signalling in response to microbes is a relatively new area of research. In this article, we discuss present knowledge of stomatal regulation in response to microbes and highlight common points of convergence, and differences, compared to stomatal regulation by abiotic stresses. We also expand on the mechanisms by which pathogens manipulate these processes to promote disease, for example by delivering effectors to inhibit closure or trigger opening of stomata. The study of pathogen effectors in stomatal manipulation will aid our understanding of guard cell signalling.


Via Nicolas Denancé, Jim Alfano
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Storify: #MPMI2014 Day 5 of XVI IC-MPMI, Rhodes, Greece, 6-10 July

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Storify: #MPMI2014 Day 3 of XVI IC-MPMI, Rhodes, Greece, 6-10 July

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Jean-Michel Ané's curator insight, July 9, 5:27 AM

I am so disappointed to miss this conference...

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Storify Archive of #OMGN14 Oomycete Molecular Genetics Network Annual Meeting, Norwich, UK, July 2-4 2014

Tweets from the Oomycete Molecular Genetics Network Annual Meeting, Norwich, UK, July 2-4 2014 http://omgn.org
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Plant J: Powdery mildew resistance gene Pm8 derived from rye is suppressed by its wheat ortholog Pm3 (2014)

Plant J: Powdery mildew resistance gene Pm8 derived from rye is suppressed by its wheat ortholog Pm3 (2014) | Plants and Microbes | Scoop.it

The powdery mildew resistance gene Pm8 derived from rye is located on a 1BL.1RS chromosome translocation in wheat. However, some wheat lines with this translocation do not show resistance to isolates of the wheat powdery mildew pathogen avirulent to Pm8 due to an unknown genetically dominant suppression mechanism. Here we show that lines with suppressed Pm8 activity contain an intact and expressedPm8 gene. Therefore, the absence of Pm8 function in certain 1BL.1RS containing wheat lines is not the result of gene loss or mutation but is based on suppression. The wheat gene Pm3, an ortholog of rye Pm8, suppressed Pm8-mediated mildew resistance in lines containing Pm8 in a transient single-cell expression assay. This result was further confirmed in transgenic lines with combined Pm8 and Pm3 transgenes. Expression analysis revealed that suppression is not the result of gene silencing, either in wheat 1BL.1RS translocation lines carrying Pm8 or in transgenic genotypes with both Pm8 and Pm3 alleles. In addition, a similar abundance of the PM8 and PM3 proteins in single or double homozygous transgenic lines suggested that a post-translational mechanism is involved in Pm8 suppression. Co-expression of Pm8 and Pm3genes in N. benthamiana leaves followed by co-immunoprecipitation analysis showed that the two proteins interact. Therefore, the formation of a heteromeric protein complex might result in inefficient or absent signal transmission for defense reaction. These data provide a molecular explanation for resistance gene suppression in certain genetic backgrounds and suggest ways to circumvent it in future plant breeding.

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PBS: The next Green Revolution may rely on microbes (2014)

PBS: The next Green Revolution may rely on microbes (2014) | Plants and Microbes | Scoop.it

Ian Sanders wants to feed the world. A soft-spoken Brit, Sanders studies fungus genetics in a lab at the University of Lausanne in Switzerland. But fear not, he’s not on a mad-scientist quest to get the world to eat protein pastes made from ground-up fungi. Still, he believes—he’s sure—that these microbes will be critical to meeting the world’s future food needs.


Sanders’s eyes widen with delight and almost childlike glee when he talks about a microscopic life form called mycorrhizal fungus, his chosen lifetime research subject. Mycorrhizal fungi live in a tightly wound, mutually beneficial embrace with most plants on the planet. Years of dedication have made Sanders into one of the world’s foremost experts on the genetics of the microbe, and he recently was part of a team that sequenced the first mycorrhizal fungi genome.


Despite his drive, Sanders comes across as light-hearted as he teases and jokes with fellow researchers. But he loses his affable smile as he fires off facts about the upcoming food shortage: The world’s population is expected to increase to between 9 billion and 16 billion people. Five million people per year die of direct causes of malnutrition. Three and a half million of those are children under five. Today, we have the means to grow enough food to feed all those people, but we will most certainly need to produce more in the very near future.


Sanders may have come up with a way to do just that. He has successfully bred custom varieties of microbes that can help plants produce more food. It’s one of the ultimate goals of farming research—more food with, he hopes, little or no environmental downside.


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Plant J: The powdery mildew resistance protein RPW8.2 is carried on VAMP721/722 vesicles to the extrahaustorial membrane of haustorial complexes (2014)

Plant J: The powdery mildew resistance protein RPW8.2 is carried on VAMP721/722 vesicles to the extrahaustorial membrane of haustorial complexes (2014) | Plants and Microbes | Scoop.it

Plants employ multiple cell-autonomous defense mechanisms to impede pathogenesis of microbial intruders. Previously we identified an exocytosis defense mechanism in Arabidopsis against pathogenic powdery mildew fungi. This pre-invasive defense mechanism depends on the formation of ternary protein complexes consisting of the plasma membrane-localized PEN1 syntaxin, the adaptor protein SNAP33, and closely sequence-related vesicle-resident VAMP721 or VAMP722 proteins. The Arabidopsis thaliana resistance to powdery mildew 8.2 protein (RPW8.2) confers disease resistance against powdery mildews upon fungal entry into host cells and is specifically targeted to the extrahaustorial membrane (EHM), which envelops the haustorial complex of the fungus. However, the secretory machinery involved in trafficking RPW8.2 to the EHM is unknown. Here we report that RPW8.2 is transiently located on VAMP721/722 vesicles, and later incorporated into the EHM of mature haustoria. RPW8.2 resistance activity against the powdery mildew Golovinomyces orontii is greatly diminished in the absence of VAMP721 but only slightly in the absence of VAMP722. Consistent with this result, trafficking of RPW8.2 to the EHM is delayed in the absence of VAMP721. These findings implicate VAMP721/722 vesicles as key components of the secretory machinery for carrying RPW8.2 to the plant-fungal interface. Quantitative fluorescence recovery after photobleaching suggests that vesicle-mediated trafficking of RPW8.2-YFP to the EHM occurs transiently during early haustorial development and that RPW8.2-YFP lateral diffusion within the EHM exceeds vesicle-mediated RPW8.2-YFP replenishment in mature haustoria. Our findings imply the engagement of VAMP721/722 in a bifurcated trafficking pathway for pre-invasive defense at the cell periphery and post-invasive defense at the EHM.

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Rakesh Yashroy's curator insight, July 2, 8:08 AM

Membrane vesicle trafficking - the 2013 Nobel winning eukaryote cell phenomenon -  is now turning out to be universal, including bacteria @ http://en.wikipedia.org/wiki/Membrane_vesicle_trafficking