There is a large diversity of genetically defined resistance genes in bread wheat against the powdery mildew pathogen Blumeria graminis (B. g.) f. sp. tritici. Many confer race-specific resistance to this pathogen, but until now only the mildew avirulence gene AvrPm3a2/f2 that is recognized by Pm3a/f was known molecularly.
We performed map-based cloning and genome-wide association studies to isolate a candidate for the mildew avirulence gene AvrPm2. We then used transient expression assays in Nicotiana benthamiana to demonstrate specific and strong recognition of AvrPm2 by Pm2.
The virulent AvrPm2 allele arose from a conserved 12 kb deletion, while there is no protein sequence diversity in the gene pool of avirulent B. g. tritici isolates. We found one polymorphic AvrPm2 allele in B. g. triticale and one orthologue in B. g. secalis and both are recognized by Pm2. AvrPm2 belongs to a small gene family encoding structurally conserved RNase-like effectors, including Avra13 from B. g. hordei, the cognate Avr of the barley resistance gene Mla13.
These results demonstrate the conservation of functional avirulence genes in two cereal powdery mildews specialized on different hosts, thus providing a possible explanation for successful introgression of resistance genes from rye or other grass relatives to wheat.
Autophagy functions as an antiviral mechanism against geminiviruses in plants. Haxim Y, Ismayil A, Jia Q, Wang Y, Zheng X, Chen T, Qian L, Liu N, Wang Y, Shaojie H, Cheng J, Yijun Q, Hong Y, Liu Y. https://elifesciences.org/content/6/e23897
Ground-breaking research over recent decades has established that secreted proteins and small molecules, termed effectors, serve important functions to support the interactions of diverse organisms with their plant hosts. Studies focused on effectors have revealed key virulence and avirulence mechanisms, and have provided new insights into the functions of plant regulatory networks, and have informed long-standing questions about host-microbe co-evolution. This fundamental understanding also holds clear implications for management of disease in crops. However, much remains to be learned, and effector biology is one of the most vibrant areas of research in the molecular plant-microbe field.
We invite research and perspective articles that explore all aspects of effector structure, function, and evolution, encompassing the full breadth of plant-associated organisms. Articles highlighting translational research as well as fundamental understanding are welcome. We look forward to assembling an issue that highlights some of the best current research in this rapidly advancing area!
The rice gene Xa4 encodes a wall-associated kinase and controls disease resistance and mechanical strength, possibly through a common mechanism.
Crop plants experience a wide range of stresses that negatively affect their performance. Rice, one of the most important global crops, is the main calorie source for more than half of the global population. Two of the major constraints in rice cultivation are bacterial diseases and lodging (Fig. 1). In this issue of Nature Plants, Hu and colleagues unravel the identity and molecular function of the Xa4 gene1. This important diseaseresistance gene codes for a wall-associated kinase (WAK). The presence of Xa4 confers resistance to bacterial blight and was found to strengthen the cell wall, which is a primary entry point for pathogens. Interestingly, cell wall reinforcement also led to reduced height of Xa4-expressing plants, thereby increasing lodging resistance. Hence, this gene has a beneficial effect on multiple agronomic traits, which can explain its importance and widespread use in rice breeding.
The last 20 years have provided a sophisticated understanding of how plants recognise relatively conserved microbial patterns to activate defence. In recent years DNA sequencing allowed genomes and transcriptomes of eukaryotic rusts and mildew pathogens to be studied and high-throughput imaging permit the study and visualisation of intracellular interactions during pathogenesis and defence.
We will present many aspects of plant microbe interactions including:
intra-cellular interactions with high-throughput imaging technology
mechanistic understanding of cellular and molecular processes to translational activities
The focus on the dynamic and interactive practical sessions will naturally promote strong interactions between lecturers and participants.
The self-association of Toll/interleukin-1 receptor/resistance protein (TIR) domains has been implicated in signaling in plant and animal immunity receptors. Structure-based studies identified different TIR-domain dimerization interfaces required for signaling of the plant nucleotide-binding oligomerization domain-like receptors (NLRs) L6 from flax and disease resistance protein RPS4 from Arabidopsis. Here we show that the crystal structure of the TIR domain from the Arabidopsis NLR suppressor of npr1-1, constitutive 1 (SNC1) contains both an L6-like interface involving helices αD and αE (DE interface) and an RPS4-like interface involving helices αA and αE (AE interface). Mutations in either the AE- or DE-interface region disrupt cell-death signaling activity of SNC1, L6, and RPS4 TIR domains and full-length L6 and RPS4. Self-association of L6 and RPS4 TIR domains is affected by mutations in either region, whereas only AE-interface mutations affect SNC1 TIR-domain self-association. We further show two similar interfaces in the crystal structure of the TIR domain from the Arabidopsis NLR recognition of Peronospora parasitica 1 (RPP1). These data demonstrate that both the AE and DE self-association interfaces are simultaneously required for self-association and cell-death signaling in diverse plant NLRs.
Several fungal plant pathogens induce ‘pseudoflowers’ on their hosts to facilitate insect-mediated transmission of gametes and spores. When spores must be transmitted to host flowers to complete the fungal life cycle, we predict that pseudoflowers should evolve traits that mimic flowers and attract the most effective vectors in the flower-visiting community. We quantified insect visitation to flowers, healthy leaves and leaves infected with Monilinia vaccinii-corymbosi(Mvc), the causative agent of mummy berry disease of blueberry. We developed a nested PCR assay for detecting Mvc spores on bees, flies and other potential insect vectors. We also collected volatiles from blueberry flowers, healthy leaves and leaves infected with Mvc, and experimentally manipulated specific pathogen-induced volatiles to assess attractiveness to potential vectors. Bees and flies accounted for the majority of contacts with flowers, leaves infected with Mvc and healthy leaves. Flowers were contacted most often, while there was no difference between bee or fly contacts with healthy and infected leaves. While bees contacted flowers more often than flies, flies contacted infected leaves more often than bees. Bees were more likely to have Mvc spores on their bodies than flies, suggesting that bees may be more effective vectors than flies for transmitting Mvc spores to flowers. Leaves infected with Mvc had volatile profiles distinct from healthy leaves but similar to flowers. Two volatiles produced by flowers and infected leaves, cinnamyl alcohol and cinnamic aldehyde, were attractive to bees, while no volatiles manipulated were attractive to flies or any other insects. These results suggest that Mvc infection of leaves induces mimicry of floral volatiles, and that transmission occurs primarily via bees, which had the highest likelihood of carrying Mvc spores and visited flowers most frequently.
Programmed cell death (PCD) mediated by mitochondrial processes has emerged as an important mechanism for plant development and responses to abiotic and biotic stress. However, the role of translocation of cytochrome c from the mitochondria to the cytosol during PCD remains unclear. Here, we demonstrate that the rice dynamin-related protein 1E (OsDRP1E) negatively regulates PCD by controlling mitochondrial structure and cytochrome c release. We used a map-based cloning strategy to isolate OsDRP1E from the lesion mimic mutant dj-lm and confirmed that the E409V mutation in OsDRP1E causes spontaneous cell death in rice. Pathogen inoculation showed that dj-lm significantly enhances resistance to fungal and bacterial pathogens. Functional analysis of the E409V mutation showed that the mutant protein impairs OsDRP1E self-association and formation of a higher-order complex; this in turn reduces the GTPase activity of OsDRP1E. Furthermore, confocal microscopy showed that the E409V mutation impairs localization of OsDRP1E to the mitochondria. The E409V mutation significantly affects the morphogenesis of cristae in the mitochondria and causes the abnormal release of cytochrome c from the mitochondria into the cytoplasm. Taken together, our results demonstrate that the mitochondria-localized protein OsDRP1E functions as a negative regulator of cytochrome c release and PCD in plants.
On behalf of the Organizing Committee, we sincerely invite colleagues to attend the 5th International Conference on Biotic Plant Interactions (5th ICBPI) in Xiamen, China on August 17-21, 2017. The theme of this five-day conference is Biotic-Plant Interactions and Sustainable Control of Pests on Crops. As a continuing effort after the 1st conference (Brisbane, Australia in 2008), the 2nd conference (Kunming, China in 2011), the 3rd conference (Yanglin, China in 2013), and the 4th conference (Nanjing, China in 2015), this conference will be organized by the State Key Laboratory of Ecological Pest Control of Fujian and Taiwan Crops, Fujian Agriculture and Forestry University and Institute of Plant Physiology and Ecology at Chinese Academy of Science, Chinese Society for Plant Biology and Chinese Society for Plant Pathology. It will bring together 800-1000 scientists all over the world and cover nine sessions: plant-fungus interactions, plant-oomycete interactions, plant-bacteria interactions, plant-virus interactions, plant-insect interactions, parasitic plants/nematodes, plant symbiosis, epigenetics in biotic plant interactions, and molecular design in crop resistance.
We are looking forward to welcoming you in Xiamen, China.
Understanding evolution of plant immunity is necessary to inform rational approaches for genetic control of plant diseases. The plant immune system is innate, encoded in the germline, yet plants are capable of recognizing diverse rapidly evolving pathogens. Plant immune receptors (NLRs) can gain pathogen recognition through point mutation, recombination of recognition domains with other receptors, and through acquisition of novel integrated protein domains. The exact molecular pathways that shape immune repertoire including new domain integration remain unknown. Here, we describe a non-uniform distribution of integrated domains among NLR subfamilies in grasses and identify genomic hotspots that demonstrate rapid expansion of NLR gene fusions. We show that just one clade in the Poaceae is responsible for the majority of unique integration events. Based on these observations we propose a model for the expansion of integrated domain repertoires that involves a flexible NLR acceptor that is capable of fusion to diverse domains derived across the genome. The identification of a subclass of NLRs that is naturally adapted to new domain integration can inform biotechnological approaches for generating synthetic receptors with novel pathogen traps.
In agricultural systems, major (R) genes for resistance in plants exert strong selection pressure on cognate/corresponding avirulence effector genes of phytopathogens. However, a complex interplay often exists between trade-offs linked to effector function and the need to escape R gene recognition. Here, using the Leptosphaeria maculans–oilseed rape pathosystem we review evolution of effectors submitted to multiple resistance gene selection. Characteristics of this pathosystem include a crop in which resistance genes have been deployed intensively resulting in ‘boom and bust’ cycles; a fungal pathogen with a high adaptive potential in which seven avirulence genes are cloned and for which population surveys have been coupled with molecular analysis of events responsible for virulence. The mode of evolution of avirulence genes, all located in dispensable parts of the ‘two-speed’ genome, is a highly dynamic gene-specific process. In some instances, avirulence genes are readily deleted under selection. However, others, even when located in the most plastic genome regions, undergo only limited point mutations or their avirulence phenotype is ‘camouflaged’ by another avirulence gene. Thus, while hundreds of effector genes are present, some effectors are likely to have an important and nonredundant function, suggesting functional redundancy and dispensability of effectors might not be the rule.
Nucleotide-binding domain and leucine-rich repeat proteins (NLRs) are important receptors in plant immunity that allow recognition of pathogen effectors. The rice NLR RGA5 recognizes the Magnaporthe oryzae effector AVR-Pia through direct interaction. Here, we gained detailed insights into the molecular and structural bases of AVR-Pia-RGA5 interaction and the role of the RATX1 decoy domain of RGA5. NMR titration combined with in vitro and in vivo protein-protein interaction analyses identified the AVR-Pia interaction surface that binds to the RATX1 domain. Structure-informed AVR-Pia mutants showed that, although AVR-Pia associates with additional sites in RGA5, binding to the RATX1 domain is necessary for pathogen recognition, but can be of moderate affinity. Therefore, RGA5-mediated resistance is highly resilient to mutations in the effector. We propose a model that explains such robust effector recognition as a consequence, and an advantage, of the combination of integrated decoy domains with additional independent effector-NLR interactions.
For the past century, plant virology and the American Phytopathological Society have a deeply intertwined history. As the Society emerged as a distinct entity in the first decade of the 20th century, viruses were also making their mark as newly described and discovered agents of disease. Interestingly, Tobacco mosaic virus (TMV) and its economic hosts in the Solanaceae, such as tobacco and tomato, also find their origins in the Americas.
What follows is a brief review of the origins of our understanding of “the nature of the virus,” deciphering the basis of host-pathogen interaction, and vignettes of the early TMV workers who developed many of the tools and techniques that have become part of the definition of what it is “to be” a virologist or “to do” virology. As plant molecular virology has its origins in the early 20th century, first from the early descriptive work of viruses diseases (1900-1935), followed by the biochemical, the genetics, and biophysical work (1935-1960), the molecular biology (1960-1980), and our current era of transgenic technology, functional genetics of plant viruses, and using viruses as molecular tools, it is useful to develop a contextual understanding of how we came to work with TMV.
Plants possess intracellular immune receptors designated “nucleotide-binding domain and leucine-rich repeat” (NLR) proteins that translate pathogen-specific recognition into disease-resistance signaling. The wheat immune receptors Sr33 and Sr50 belong to the class of coiled-coil (CC) NLRs. They confer resistance against a broad spectrum of field isolates of Puccinia graminis f. sp. tritici, including the Ug99 lineage, and are homologs of the barley powdery mildew-resistance protein MLA10. Here, we show that, similarly to MLA10, the Sr33 and Sr50 CC domains are sufficient to induce cell death in Nicotiana benthamiana. Autoactive CC domains and full-length Sr33 and Sr50 proteins self-associate in planta. In contrast, truncated CC domains equivalent in size to an MLA10 fragment for which a crystal structure was previously determined fail to induce cell death and do not self-associate. Mutations in the truncated region also abolish self-association and cell-death signaling. Analysis of Sr33 and Sr50 CC domains fused to YFP and either nuclear localization or nuclear export signals in N. benthamiana showed that cell-death induction occurs in the cytosol. In stable transgenic wheat plants, full-length Sr33 proteins targeted to the cytosol provided rust resistance, whereas nuclear-targeted Sr33 was not functional. These data are consistent with CC-mediated induction of both cell-death signaling and stem rust resistance in the cytosolic compartment, whereas previous research had suggested that MLA10-mediated cell-death and disease resistance signaling occur independently, in the cytosol and nucleus, respectively.
Plant associated microbes rely on secreted virulence factors (effectors) to modulate host immunity and ensure progressive infection. Amongst the secreted protein repertoires defined and studied in pathogens to date, the CRNs (for CRinkling and Necrosis) have emerged as one of only a few highly conserved protein families, spread across several kingdoms. CRN proteins were first identified in plant pathogenic oomycetes where they were found to be modular factors that are secreted and translocated inside host cells by means of a conserved N-terminal domain. Subsequent localization and functional studies have led to the view that CRN C-termini execute their presumed effector function in the host nucleus, targeting processes required for immunity. These findings have led to great interest in this large protein family and driven the identification of additional CRN-like proteins in other organisms. The identification of CRN proteins and subsequent functional studies have markedly increased the number of candidate CRN protein sequences, expanded the range of phenotypes tentatively associated with function and revealed some of their molecular functions towards virulence. The increased number of characterised CRNs also has presented a set of challenges that may impede significant progress in the future. Here, we summarise our current understanding of the CRNs and re-assess some basic assumptions regarding this protein family. We will discuss the latest findings on CRN biology and highlight exciting new hypotheses that have emanated from the field. Finally, we will discuss new approaches to study CRN functions that would lead to a better understanding of CRN effector biology as well as the processes that lead to host susceptibility and immunity.
iMMM2017 Research into the molecular basis of symbiosis between plant roots and fungi has achieved major breakthroughs in recent years. The international Molecular Mycorrhiza Meeting (iMMM) is a response to the perceived need for a specialized meeting series covering the molecular mechanistic aspects of mycorrhizal symbioses including yet non-categorised endophytic root fungus interactions. After the success of the two first editions in Munich (2012) and Cambridge (2015), the 3rd international Molecular Mycorrhiza Meeting will be held in Toulouse in 2017. To keep the meeting highly interactive, the participant number will be limited to 150 people.
Background. The prevailing paradigm of host-parasite evolution is that arms races lead to increasing specialisation via genetic adaptation. Insect herbivores are no exception and the majority have evolved to colonise a small number of closely related host species. Remarkably, the green peach aphid, Myzus persicae, colonises plant species across 40 families and single M. persicae clonal lineages can colonise distantly related plants. This remarkable ability makes M. persicae a highly destructive pest of many important crop species.
Results. To investigate the exceptional phenotypic plasticity of M. persicae, we sequenced the M. persicae genome and assessed how one clonal lineage responds to host plant species of different families. We show that genetically identical individuals are able to colonise distantly related host species through the differential regulation of genes belonging to aphid-expanded gene families. Multigene clusters collectively upregulate in single aphids within two days upon host switch. Furthermore, we demonstrate the functional significance of this rapid transcriptional change using RNA interference (RNAi)-mediated knock-down of genes belonging to the cathepsin B gene family. Knock-down of cathepsin B genes reduced aphid fitness, but only on the host that induced upregulation of these genes.
Conclusions. Previous research has focused on the role of genetic adaptation of parasites to their hosts. Here we show that the generalist aphid pest M. persicae is able to colonise diverse host plant species in the absence of genetic specialisation. This is achieved through rapid transcriptional plasticity of genes that have duplicated during aphid evolution.
Detection of pathogens by plants is mediated by intracellular nucleotide-binding site leucine-rich repeat (NLR) receptor proteins. NLR proteins are defined by their stereotypical multidomain structure: an N-terminal Toll–interleukin receptor (TIR) or coiled-coil (CC) domain, a central nucleotide-binding (NB) domain, and a C-terminal leucine-rich repeat (LRR). The plant innate immune system contains a limited NLR repertoire that functions to recognize all potential pathogens. We isolated Response to the bacterial type III effector protein HopBA1 (RBA1), a gene that encodes a TIR-only protein lacking all other canonical NLR domains. RBA1 is sufficient to trigger cell death in response to HopBA1. We generated a crystal structure for HopBA1 and found that it has similarity to a class of proteins that includes esterases, the heme-binding protein ChaN, and an uncharacterized domain of Pasteurella multocida toxin. Self-association, coimmunoprecipitation with HopBA1, and function of RBA1 require two previously identified TIR–TIR dimerization interfaces. Although previously described as distinct in other TIR proteins, in RBA1 neither of these interfaces is sufficient when the other is disrupted. These data suggest that oligomerization of RBA1 is required for function. Our identification of RBA1 demonstrates that “truncated” NLRs can function as pathogen sensors, expanding our understanding of both receptor architecture and the mechanism of activation in the plant immune system.
The 16th International Conference on Pseudomonas will take place at St George's Hall in Liverpool, UK.
The Pseudomonas International Conference is a biennial event that brings together researchers from all over the world who are working on the genus Pseudomonas, including not only the important human pathogen Pseudomonas aeruginosa, but also a range of other important species with relevance to plant pathogenicity, bioremediation and environmental microbiology. It is also a group of organisms used widely for the study of host–pathogen interactions; cell–cell communication systems; evolutionary biology; gene regulation and metabolic networks; secretion systems; antibiotics (and resistance); bioremediation; biofilms; bacterial genomics; and other topics of broader relevance to microbiology and molecular biology generally.
The meeting is aimed primarily at scientists (from postgraduate students to PIs) with an interest in Pseudomonas, but because of the widespread use of this genus as a model to study multiple systems, it will be of general interest to other researchers active in areas such as evolutionary biology, communication systems, genomics and biofilm research. In addition, because P. aeruginosa is a key pathogen associated with both acute and chronic infections, and particularly important in the context of cystic fibrosis and antimicrobial resistance, the meeting will be of interest to clinicians and clinical researchers.
Filamentous plant pathogens and symbionts invade their host cells but remain enveloped by host-derived membranes. The mechanisms underlying the biogenesis and functions of these host-microbe interfaces are poorly understood. Recently, we showed that PexRD54, an effector from the Irish potato famine pathogen Phytophthora infestans, binds host protein ATG8CL to stimulate autophagosome formation and deplete the selective autophagy receptor Joka2 from ATG8CL complexes. Here, we show that during P. infestans infection, ATG8CL autophagosomes are diverted to the pathogen interface. Our findings are consistent with the view that the pathogen coopts host selective autophagy for its own benefit.
Cullin3-based RING E3 ubiquitin ligases (CRL3), composed of Cullin3 (CUL3), RBX1, and BTB proteins, are involved in plant immunity but the function of CUL3 in the process is largely unknown. Here, we show that rice OsCUL3a is important for the regulation of cell death and immunity. The rice lesion mimic mutant oscul3a displays a significant increase in the accumulation of flg22- and chitin-induced reactive oxygen species, and in pathogenesis-related gene expression as well as resistance to Magnaporthe oryzae and Xanthomonas oryzae pv. oryzae. We cloned the OsCUL3a gene via a map-based strategy and found that the lesion mimic phenotype of oscul3a is associated with the early termination of OsCUL3a protein. Interaction assays showed that OsCUL3a interacts with both OsRBX1a and OsRBX1b to form a multi-subunit CRL in rice. Strikingly, OsCUL3a interacts with and degrades OsNPR1, which acts as a positive regulator of cell death in rice. Accumulation of OsNPR1 protein is greater in the oscul3a mutant than in the wild type. Furthermore, the oscul3a osnpr1 double mutant does not exhibit the lesion mimic phenotype of the oscul3a mutant. Our data demonstrate that OsCUL3a negatively regulates cell death and immunity by degrading OsNPR1 in rice.
In this commentary I question the wisdom and efficacy of studies seeking disease attenuating microbes and microbiomes only in healthy plant communities and posit the alternative view that success in biocontrol of crop diseases may come also come from studies of microbiota, or at least individual species isolates, associated with diseased plants. In support of this view I summarise the current extensive knowledge of the biology behind what is probably the most successful biocontrol of a plant disease, namely the biocontrol of crown gall of stone fruit using non-pathogenic Rhizobium rhizogenes strain K84 (New and Kerr, 1972; Kerr, 2016) where the biocontrol agent itself came from a diseased plant.
In plants, perception of invading pathogens involves cell-surface immune receptor kinases. Here, we report that the Arabidopsis SITE-1 PROTEASE (S1P) cleaves endogenous RAPID ALKALINIZATION FACTOR (RALF) propeptides to inhibit plant immunity. This inhibition is mediated by the malectin-like receptor kinase FERONIA (FER), which otherwise facilitates the ligand-induced complex formation of the immune receptor kinases EF-TU RECEPTOR (EFR) and FLAGELLIN-SENSING 2 (FLS2) with their co-receptor BRASSINOSTEROID INSENSITIVE 1–ASSOCIATED KINASE 1 (BAK1) to initiate immune signaling. We show that FER acts as a RALF-regulated scaffold that modulates receptor kinase complex assembly. A similar scaffolding mechanism may underlie FER function in other signaling pathways.Empty description
Steroidal alkaloids (SAs) and their glycosylated forms (SGAs) are toxic compounds largely produced by members of the Solanaceae and Liliaceae plant families. This class of specialized metabolites serves as a chemical barrier against a broad range of pest and pathogens. In humans and animals, SAs are considered anti-nutritional factors because they affect the digestion and absorption of nutrients from food and might even cause poisoning. In spite of the first report on SAs nearly 200 years ago, much of the molecular basis of their biosynthesis and regulation remains unknown. Aspects concerning chemical structures and biological activities of SAs have been reviewed extensively elsewhere; therefore, in this review the latest insights to the elucidation of the SAs biosynthetic pathway are highlighted. Recently, co-expression analysis combined with metabolic profiling revealed metabolic gene clusters in tomato and potato that contain core genes required for production of the prominent SGAs in these two species. Elaborating the knowledge regarding the SAs biosynthetic pathway, the subcellular transport of these molecules, as well as the identification of regulatory and signaling factors associated with SA metabolism will likely advance understanding of chemical defense mechanisms in Solanaceae and Liliaceae plants. It will also provide the means to develop, through classical breeding or genetic engineering, crops with modified levels of anti-nutritional SAs.
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