Xanthomonas campestris pathovar campestris causes black rot, a vascular disease on cruciferous plants, including Arabidopsis thaliana. The gene XC1553 from X. campestris pv. campestris strain 8004 encodes a protein containing leucine-rich repeats (LRRs) and appears to be restricted to strains of X. campestris pv. campestris. LRRs are found in a number of type III-secreted effectors in plant and animal pathogens. These prompted us to investigate the role of the XC1553 gene in the interaction between X. campestris pv. campestris and A. thaliana. Translocation assays using the hypersensitive-reaction-inducing domain of X. campestris pv. campestris AvrBs1 as a reporter revealed that XC1553 is a type III effector. Infiltration of Arabidopsis leaf mesophyll with bacterial suspensions showed no differences between the wild-type strain and an XC1553 gene mutant; both strains induced disease symptoms on Kashmir and Col-0 ecotypes. However, a clear difference was observed when bacteria were introduced into the vascular system by piercing the central vein of leaves. In this case, the wild-type strain 8004 caused disease on the Kashmir ecotype, but not on ecotype Col-0; the XC1553 gene mutant became virulent on the Col-0 ecotype and still induced disease on the Kashmir ecotype. Altogether, these data show that the XC1553 gene, which was renamed avrACXcc8004, functions as an avirulence gene whose product seems to be recognized in vascular tissues.
This workshop aims to draw together researchers in plant and animal NLR biology to discuss recent conceptual advances and future directions for the field. The workshop will take place at Schloss Ringberg in Bavaria, Germany from May 3–6, 2015. View the workshop poster for more information on how to register and submit an abstract.
A cluster of three rice lectin receptor kinases confers resistance to planthopper insects.
Insect pests reduce yields of crops worldwide through direct damage and because they spread devastating viral diseases. In Asia, the brown planthopper (BPH) decimates rice (Oryza sativa) crops, causing the loss of billions of dollars annually1. In this issue, Liu et al.2 report the cloning of a rice genetic locus that confers broad-spectrum resistance to BPH and at least one other planthopper species (white back planthopper). Introducing this locus into plant genomes is likely to provide an effective means of combating insect pests of rice and of other cereals such as maize.
In modern rice agriculture, BPH damage is controlled through breeding and the application of vast amounts of chemical pesticides1. Pesticides are not a sustainable approach, however, owing to high costs, harmful environmental effects and rapid development of resistant insects. Breeding programs have identified more than 20 genetic loci in cultivated or wild rice species that confer BPH resistance1. However, these Bph loci are usually only effective against specific BPH biotypes, and newly evolved BPH populations have rapidly overcome several Bph resistance loci deployed in the field..
Of the >20 identified Bph loci, only Bph14 and Bph26 have been cloned. Both of these loci encode coiled-coil, nucleotide-binding and leucine-rich repeat proteins3, 4, the main class of plant intracellular immune receptors5. Bph3 is a resistance locus that was first pinpointed genetically in the Sri Lankan rice indica cultivar Rathu Heenati. Notably, unlike most other Bph loci, including Bph14 and Bph26, Bph3 confers broad-spectrum resistance to many BPH biotypes as well as to the white back planthopper1, 2. The success of Bph3 as a resistance locus might be linked to the fact that it acts against BPH at an early stage of the feeding cycle, before the insect can deploy its arsenal of virulence proteins that circumvent plant defenses.
Despite the huge potential of Bph3 for rice agriculture, its molecular identity has been unknown. Liu et al.2 now identify Bph3 through map-based cloning in a cross between the resistant indica cultivar Rathu Heenati and the susceptible japonica cultivar 02428. Bph3 maps to a 79-kb genomic region that contains a cluster of three lectin receptor kinases, OsLecRK1–3 (ref. 2) (Fig. 1). The authors find that single-nucleotide polymorphisms in these genes are associated with BPH resistance in different cultivated rice accessions. They also show that ectopic expression of the OsLecRK1–3 gene cluster in the susceptible japonica Kitaake cultivar confers BPH resistance.
Mitogen-activated protein kinase (MAPK) cascades play central roles in innate immune signalling networks in plants and animals1, 2. In plants, however, the molecular mechanisms of how signal perception is transduced to MAPK activation remain elusive1. Here we report that pathogen-secreted proteases activate a previously unknown signalling pathway in Arabidopsis thaliana involving the Gα, Gβ, and Gγ subunits of heterotrimeric G-protein complexes, which function upstream of an MAPK cascade. In this pathway, receptor for activated C kinase 1 (RACK1) functions as a novel scaffold that binds to the Gβ subunit as well as to all three tiers of the MAPK cascade, thereby linking upstream G-protein signalling to downstream activation of an MAPK cascade. The protease–G-protein–RACK1–MAPK cascade modules identified in these studies are distinct from previously described plant immune signalling pathways such as that elicited by bacterial flagellin, in which G proteins function downstream of or in parallel to an MAPK cascade without the involvement of the RACK1 scaffolding protein. The discovery of the new protease-mediated immune signalling pathway described here was facilitated by the use of the broad host range, opportunistic bacterial pathogen Pseudomonas aeruginosa. The ability of P. aeruginosa to infect both plants and animals makes it an excellent model to identify novel immunoregulatory strategies that account for its niche adaptation to diverse host tissues and immune systems.
The 2015 Molecular Biology of Plant Pathogens (MBPP) conference will be held at the University of the West of England (UWE), Bristol on the 8th-9th April 2015. This will be the 23rd MBPP conference!
UWE is the largest university in the South West of England with over 30,000 students and approximately 3,500 staff. UWE has a long and interesting history starting life as a Merchant Venturer’s Navigation College in 1595 and undergoing many changes before gaining University status in 1992. Today UWE attracts students from all over the UK as well as a significant number of international students from 140 countries worldwide.
UWE has an active research community which makes a significant contribution to advances in industry, commerce, health and technology both nationally and internationally. The organisers of this years’ MBPP conference, Professor Dawn Arnold, Dr Carrie Brady and Dr Helen Neale work within the Centre for Research in Bioscience (CRIB) which leads world-class research in areas of strategic importance including plant science, agri-food, bio-sensing and biomedicine.
MBPP provides an excellent forum for networking between junior and senior scientists. The primary focus is on providing PhD students and post-doctoral scientists the opportunity to give oral presentations in front of a wide range of national and international researchers.
There will also be three keynote talks by internationally renowned scientists Professor Pietro Spanu (Imperial College), Dr Chris Ridout (John Innes Centre) and Professor Teresa Coutinho (Forestry and Agricultural Biotechnology Institute, University of Pretoria, South Africa). Please see our biographies tab for more information on these speakers.
Plant disease resistance is often mediated by nucleotide binding-leucine rich repeat (NLR) proteins which remain auto-inhibited until recognition of specific pathogen-derived molecules causes their activation, triggering a rapid, localized cell death called a hypersensitive response (HR). Three domains are recognized in one of the major classes of NLR proteins: a coiled-coil (CC), a nucleotide binding (NB-ARC) and a leucine rich repeat (LRR) domains. The maize NLR gene Rp1-D21 derives from an intergenic recombination event between two NLR genes, Rp1-D and Rp1-dp2 and confers an autoactive HR. We report systematic structural and functional analyses of Rp1 proteins in maize and N. benthamiana to characterize the molecular mechanism of NLR activation/auto-inhibition. We derive a model comprising the following three main features: Rp1 proteins appear to self-associate to become competent for activity. The CC domain is signaling-competent and is sufficient to induce HR. This can be suppressed by the NB-ARC domain through direct interaction. In autoactive proteins, the interaction of the LRR domain with the NB-ARC domain causes de-repression and thus disrupts the inhibition of HR. Further, we identify specific amino acids and combinations thereof that are important for the auto-inhibition/activity of Rp1 proteins. We also provide evidence for the function of MHD2, a previously uncharacterized, though widely conserved NLR motif. This work reports several novel insights into the precise structural requirement for NLR function and informs efforts towards utilizing these proteins for engineering disease resistance.
We identified the Magnaporthe oryzae avirulence effector AvrPi9 cognate to rice blast resistance gene Pi9 by comparative genomics of requisite strains derived from a sequential planting method.
AvrPi9 encodes a small secreted protein that appears to localize in the biotrophic interfacial complex and is translocated to the host cell during rice infection. AvrPi9 forms a tandem gene array with its paralogue proximal to centromeric region of chromosome 7. AvrPi9 is expressed highly at early stages during initiation of blast disease.
Virulent isolate strains contain Mg-SINE within the AvrPi9 coding sequence. Loss of AvrPi9 did not lead to any discernible defects during growth or pathogenesis in M. oryzae. This study reiterates the role of diverse transposable elements as off-switch agents in acquisition of gain-of-virulence in the rice blast fungus.
The prevalence of AvrPi9 correlates well with the avirulence pathotype in diverse blast isolates from the Philippines and China, thus supporting the broad-spectrum resistance conferred by Pi9 in different rice growing areas. Our results revealed that Pi9 and Piz-t at the Pi2/9 locus activate race specific resistance by recognizing sequence-unrelated AvrPi9 and AvrPiz-t genes, respectively.
Plant-infecting viruses are transmitted by a diverse array of organisms including insects, mites, nematodes, fungi, and plasmodiophorids. Virus interactions with these vectors are diverse, but there are some commonalities. Generally the infection cycle begins with the vector encountering the virus in the plant and the virus is acquired by the vector. The virus must then persist in or on the vector long enough for the virus to be transported to a new host and delivered into the plant cell. Plant viruses rely on their vectors for breaching the plant cell wall to be delivered directly into the cytosol. In most cases, viral capsid or membrane glycoproteins are the specific viral proteins that are required for transmission and determinants of vector specificity. Specific molecules in vectors also interact with the virus and while there are few-identified to no-identified receptors, candidate recognition molecules are being further explored in these systems. Due to the specificity of virus transmission by vectors, there are defined steps that represent good targets for interdiction strategies to disrupt the disease cycle. This review focuses on new technologies that aim to disrupt the virus–vector interaction and focuses on a few of the well-characterized virus–vector interactions in the field. In closing, we discuss the importance of integration of these technologies with current methods for plant virus disease control.
Plants and plant pathogens are subject to continuous co-evolutionary pressure for dominance, and the outcomes of these interactions can substantially impact agriculture and food security1, 2, 3. In virus–plant interactions, one of the major mechanisms for plant antiviral immunity relies on RNA silencing, which is often suppressed by co-evolving virus suppressors, thus enhancing viral pathogenicity in susceptible hosts1. In addition, plants use the nucleotide-binding and leucine-rich repeat (NB-LRR) domain-containing resistance proteins, which recognize viral effectors to activate effector-triggered immunity in a defence mechanism similar to that employed in non-viral infections2, 3. Unlike most eukaryotic organisms, plants are not known to activate mechanisms of host global translation suppression to fight viruses1, 2. Here we demonstrate in Arabidopsis that the constitutive activation of NIK1, a leucine-rich repeat receptor-like kinase (LRR-RLK) identified as a virulence target of the begomovirus nuclear shuttle protein (NSP)4, 5, 6, leads to global translation suppression and translocation of the downstream component RPL10 to the nucleus, where it interacts with a newly identified MYB-like protein, L10-INTERACTING MYB DOMAIN-CONTAINING PROTEIN (LIMYB), to downregulate translational machinery genes fully. LIMYB overexpression represses ribosomal protein genes at the transcriptional level, resulting in protein synthesis inhibition, decreased viral messenger RNA association with polysome fractions and enhanced tolerance to begomovirus. By contrast, the loss of LIMYBfunction releases the repression of translation-related genes and increases susceptibility to virus infection. Therefore, LIMYB links immune receptor LRR-RLK activation to global translation suppression as an antiviral immunity strategy in plants.
Intracellular immune receptors of the nucleotide-binding leucine-rich repeat (NB-LRR or NLR) proteins often function in pairs, with "helper" proteins required for the activity of "sensors" that mediate pathogen recognition. The NLR helper NRC1 (NB-LRR protein required for HR-associated cell death 1) has been described as a signalling hub required for the cell death mediated by both cell surface and intracellular immune receptors in the model plant Nicotiana benthamiana. However, this work predates the availability of the N. benthamiana genome and whether NRC1 is indeed required for the reported phenotypes has not been confirmed. Here, we investigated the NRC family of solanaceous plants using a combination of genome annotation, phylogenetics, gene silencing and genetic complementation experiments. We discovered that a paralog of NRC1, we termed NRC3, is required for the hypersensitive cell death triggered by the disease resistance protein Pto but not Rx and Mi-1.2. NRC3 may also contribute to the hypersensitive cell death triggered by the receptor-like protein Cf-4. Our results highlight the importance of applying genetic complementation to validate gene function in RNA silencing experiments.
The ubiquitin proteasome system in plants plays important roles in plant-microbe interactions and in immune responses to pathogens. We previously demonstrated that the rice U-box E3 ligase SPL11 and its Arabidopsis ortholog PUB13 negatively regulate programmed cell death (PCD) and defense response. However, the components involved in the SPL11/PUB13-mediated PCD and immune signaling pathway remain unknown. In this study, we report that SPL11-interacting Protein 6 (SPIN6) is a Rho GTPase-activating protein (RhoGAP) that interacts with SPL11 in vitro and in vivo. SPL11 ubiquitinates SPIN6 in vitro and degrades SPIN6 in vivo via the 26S proteasome-dependent pathway. Both RNAi silencing in transgenic rice and knockout of Spin6 in a T-DNA insertion mutant lead to PCD and increased resistance to the rice blast pathogen Magnaporthe oryzae and the bacterial blight pathogen Xanthomonas oryzae pv. oryzae. The levels of reactive oxygen species and defense-related gene expression are significantly elevated in both the Spin6 RNAi and mutant plants. Strikingly, SPIN6 interacts with the small GTPase OsRac1, catalyze the GTP-bound OsRac1 into the GDP-bound state in vitro and has GAP activity towards OsRac1 in rice cells. Together, our results demonstrate that the RhoGAP SPIN6 acts as a linkage between a U-box E3 ligase-mediated ubiquitination pathway and a small GTPase-associated defensome system for plant immunity.
The perception of downy mildew avirulence (Arabidopsis thaliana Recognized[ATR]) gene products by matching Arabidopsis thaliana resistance (Recognition of Peronospora parasitica [RPP]) gene products triggers localized cell death (a hypersensitive response) in the host plant, and this inhibits pathogen development. The oomycete pathogen, therefore, is under selection pressure to alter the form of these gene products to prevent detection. That the pathogen maintains these genes indicates that they play a positive role in pathogen survival. Despite significant progress in cloning plant RPP genes and characterizing essential plant components of resistance signaling pathways, little progress has been made in identifying the oomycete molecules that trigger them. Concluding a map-based cloning effort, we have identified an avirulence gene, ATR1NdWsB, that is detected by RPP1 from the Arabidopsis accession Niederzenz in the cytoplasm of host plant cells. We report the cloning of six highly divergent alleles of ATR1NdWsB from eight downy mildew isolates and demonstrate that the ATR1NdWsB alleles are differentially recognized by RPP1 genes from two Arabidopsis accessions (Niederzenz and Wassilewskija). RPP1-Nd recognizes a single allele of ATR1NdWsB; RPP1-WsB also detects this allele plus three additional alleles with divergent sequences. The Emco5 isolate expresses an allele ofATR1NdWsB that is recognized by RPP1-WsB, but the isolate evades detection in planta. Although the Cala2 isolate is recognized by RPP1-WsA, the ATR1NdWsBallele from Cala2 is not, demonstrating that RPP1-WsA detects a novel ATR gene product. Cloning of ATR1NdWsB has highlighted the presence of a highly conserved novel amino acid motif in avirulence proteins from three different oomycetes. The presence of the motif in additional secreted proteins from plant pathogenic oomycetes and its similarity to a host-targeting signal from malaria parasites suggest a conserved role in pathogenicity.
Xanthomonas campestris pv. campestris (Xcc) colonizes the vascular system of Brassicaceaeand ultimately causes black rot. In susceptible Arabidopsis plants, XopAC type III effector inhibits by uridylylation positive regulators of the PAMP-triggered immunity such as the receptor-like cytoplasmic kinases (RLCK) BIK1 and PBL1. In the resistant ecotype Col-0, xopAC is a major avirulence gene of Xcc. In this study, we show that both the RLCK interaction domain and the uridylyl transferase domain of XopAC are required for avirulence. Furthermore, xopAC can also confer avirulence to both the vascular pathogen Ralstonia solanacearum and the mesophyll-colonizing pathogen Pseudomonas syringae indicating that xopAC-specified effector-triggered immunity is not specific to the vascular system. In planta, XopAC-YFP fusions are localized at the plasma membrane suggesting that XopAC might interact with membrane-localized proteins. Eight RLCK of subfamily VII predicted to be localized at the plasma membrane and interacting with XopAC in yeast two-hybrid assays have been isolated. Within this subfamily, PBL2 and RIPK RLCK genes but not BIK1 are important for xopAC-specified effector-triggered immunity and Arabidopsis resistance to Xcc.
Perception of pathogen (or microbe)-associated molecular patterns (PAMPs/MAMPs) by pattern recognition receptors (PRRs) is a key component of plant innate immunity. The Arabidopsis PRR EF-Tu receptor (EFR) recognizes the bacterial PAMP elongation factor Tu (EF-Tu) and its derived peptide elf18. Previous work revealed that transgenic expression of AtEFR in Solanaceae confers elf18 responsiveness and broad-spectrum bacterial disease resistance.In this study, we developed a set of bioassays to study the activation of PAMP-triggered immunity (PTI) in wheat. We generated transgenic wheat (Triticum aestivum) plants expressing AtEFR driven by the constitutive rice actin promoter and tested their response to elf18.We show that transgenic expression of AtEFR in wheat confers recognition of elf18, as measured by the induction of immune marker genes and callose deposition. When challenged with the cereal bacterial pathogen Pseudomonas syringae pv. oryzae, transgenic EFR wheat lines had reduced lesion size and bacterial multiplication.These results demonstrate that AtEFR can be transferred successfully from dicot to monocot species, further revealing that immune signalling pathways are conserved across these distant phyla. As novel PRRs are identified, their transfer between plant families represents a useful strategy for enhancing resistance to pathogens in crops.
MPMI has played a leading role in disseminating new insights into plant-microbe interactions and promoting new approaches. Articles in this Focus Issue highlight the power of genomic studies in uncovering novel determinants of plant interactions with microbial symbionts (good), pathogens (bad), and complex microbial communities (unknown). Many articles also illustrate how genomics can support translational research by quickly advancing our knowledge of important microbes that have not been widely studied.
Click on Next Article or Table of Contents above to view the articles in this Focus Issue. (From the mobile site, go to the MPMI March 2015 issue.)
Plant immunity requires recognition of pathogen effectors by intracellular NB-LRR immune receptors encoded by Resistance (R) genes. Most R proteins recognize a specific effector, but some function in pairs that recognize multiple effectors. Arabidopsis thaliana TIR-NB-LRR proteins RRS1-R and RPS4together recognize two bacterial effectors, AvrRps4 from Pseudomonas syringae and PopP2 from Ralstonia solanacearum. However, AvrRps4, but not PopP2, is recognized in rrs1/rps4 mutants. We reveal an R gene pair that resembles and is linked to RRS1/RPS4, designated as RRS1B/RPS4B, which confers recognition of AvrRps4 but not PopP2. Like RRS1/RPS4, RRS1B/RPS4B proteins associate and activate defence genes upon AvrRps4 recognition. Inappropriate combinations (RRS1/RPS4B or RRS1B/RPS4) are non-functional and this specificity is not TIR domain dependent. Distinct putative orthologues of both pairs are maintained in the genomes of Arabidopsis thalianarelatives and are likely derived from a common ancestor pair. Our results provide novel insights into paired R gene function and evolution.
Over 100 years after trypanosomatids were first discovered in plant tissues, Phytomonasparasites have now been isolated across the globe from members of 24 different plant families. Most identified species have not been associated with any plant pathology and to date only two species are definitively known to cause plant disease. These diseases (wilt of palm and coffee phloem necrosis) are problematic in areas of South America where they threaten the economies of developing countries. In contrast to their mammalian infective relatives, our knowledge of the biology of Phytomonas parasites and how they interact with their plant hosts is limited. This review draws together a century of research into plant trypanosomatids, from the first isolations and experimental infections to the recent publication of the first Phytomonas genomes. The availability of genomic data for these plant parasites opens a new avenue for comparative investigations into trypanosomatid biology and provides fresh insight into how this important group of parasites have adapted to survive in a spectrum of hosts from crocodiles to coconuts.
The spread of exotic and aggressive strains of a plant fungus is presenting a serious threat to wheat production in the UK, according to research published in Genome Biology. The research uses a new surveillance technique that could be applied internationally to respond to the spread of a wide variety of plant diseases.
Wheat is a critical staple and provides 20% of the calories and over 25% of the protein consumed by humans. 'Yellow rust' caused by the fungus Puccinia striiformis f. sp. tritici (PST) is one of the plant's major diseases and is widespread across the major wheat-producing areas of the world. Infections lead to significant reductions in both grain quality and yield, with some rare events leading to the loss of an entire crop. New fungus strains have recently emerged that adapt to warmer temperatures, are more aggressive and have overcome many of the major defensive genes in wheat.
Lead author Diane Saunders of the John Innes Centre and The Genome Analysis Centre (TGAC), UK, said: "Increased virulence, globalization, and climate change, are all increasing the scale and frequency of emerging plant diseases, and threatening global food security.
"Our research shows that in the UK we have a newly emerging population of wheat rust fungus that could be the result of an influx of more exotic and aggressive strains that are displacing the previous population. By continuing to use these new surveillance techniques, not only can we track and respond to the ongoing threat of wheat rust, but our technology opens the door for tracking other plant pathogens, including ash dieback."
Researchers from the John Innes Centre, The Sainsbury Laboratory, TGAC and the National Institute of Agricultural Botany sequenced genetic material from 39 PST-infected samples of wheat collected from 17 UK counties in 2013.
By comparing the fungal RNA with fungal genetic information from previously prevalent populations between 1978 and 2011, they showed that there has been a rapid and dramatic shift in the PST population that could have serious implications for wheat production in the UK.
The 2013 PST samples showed more genetic variation and diversity, reflecting an increase in the evolutionary potential in the UK pathogen population that could enhance their ability to overcome disease resistance in wheat.
Of the samples, 11 were also genetically similar to a PST strain called "Warrior". The strain emerged in 2011 as a serious threat to European wheat production due to its virulence on an array of previously resistant wheat varieties. This indicates that a diverse PST population containing the "Warrior" strain is now prevalent across the UK.
This new diagnostic technique, called "field pathogenomics", could be applied internationally to respond to the spread of a wide variety of plant diseases. By rapidly pinpointing a fungus's genetic make-up from field samples, the technique is able to confirm outbreaks on particular wheat varieties and provides an efficient means of confirming whether previously resistant wheat varieties have been broken by virulent strains of the pathogen. This is in contrast to current techniques which can be lengthy, costly and are only able to sample a relatively small proportion of the fungal population.
The data collection and analysis took just a few months to produce from sample collections from the field, demonstrating the potential for the method to reduce delays and transform current disease surveillance systems. The highly detailed information that is generated could help inform disease incidence predictions and agricultural practices.
Gall-forming arthropods are highly specialized herbivores that, in combination with their hosts, produce extended phenotypes with unique morphologies . Many are economically important, and others have improved our understanding of ecology and adaptive radiation . However, the mechanisms that these arthropods use to induce plant galls are poorly understood. We sequenced the genome of the Hessian fly (Mayetiola destructor; Diptera: Cecidomyiidae), a plant parasitic gall midge and a pest of wheat (Triticumspp.), with the aim of identifying genic modifications that contribute to its plant-parasitic lifestyle. Among several adaptive modifications, we discovered an expansive reservoir of potential effector proteins. Nearly 5% of the 20,163 predicted gene models matched putative effector gene transcripts present in the M. destructor larval salivary gland. Another 466 putative effectors were discovered among the genes that have no sequence similarities in other organisms. The largest known arthropod gene family (family SSGP-71) was also discovered within the effector reservoir. SSGP-71 proteins lack sequence homologies to other proteins, but their structures resemble both ubiquitin E3 ligases in plants and E3-ligase-mimicking effectors in plant pathogenic bacteria. SSGP-71 proteins and wheat Skp proteins interact in vivo. Mutations in different SSGP-71 genes avoid the effector-triggered immunity that is directed by the wheat resistance genes H6 and H9. Results point to effectors as the agents responsible for arthropod-induced plant gall formation.
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:
- gene discovery - genome analysis - 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.
Our conceptual and mechanistic understanding of how plant nucleotide-binding leucine-rich repeat (NLR or NB-LRR) proteins perceive pathogens continues to advance. NLRs are intracellular multidomain proteins that recognize pathogen-derived effectors either directly or indirectly (Jones and Dangl, 2006; van der Hoorn and Kamoun, 2008; Dodds and Rathjen, 2010; Cesari et al., 2014). In the direct model, the NLR protein binds a pathogen effector or serves as a substrate for the effector’s enzymatic activity. In the indirect model, the NLR recognizes modifications of additional host protein(s) targeted by the effector. Such intermediate host protein(s) are often called effector targets (ETs). However, given that effectors can act on multiple host targets, the specific protein that mediates recognition by the NLR may not be the effector’s operative target and may have evolved to function as a decoy dedicated to pathogen detection. This “decoy” model contrasts with the “guard” model in which the NLR perceives the effector via its action on its operative target (van der Hoorn and Kamoun, 2008).
In a recent article, Cesari et al. (2014) elegantly synthesized the literature to propose a novel model of how NLRs recognise effectors termed the “integrated decoy” hypothesis. Based on new data from several pathosystems, it appears that some NLRs recognize pathogen effectors through extraneous domains that have evolved by duplication of an ET followed by fusion into the NLR. This NLR-integrated domain mimics the effector binding/substrate property of the original ET to enable pathogen detection. In addition, these “receptor” or “sensor” NLRs typically partner with NLR proteins with a classic architecture that function as signalling partners required for the resistance response (Eitas and Dangl, 2010; Cesari et al., 2013; Cesari et al., 2014; Williams et al., 2014).
Here, we expand on the Cesari et al. (2014) model and introduce the possibility that NLR-integrated domains do not have to be decoys (as in defective mimics) of the effector’s operative target. Indeed, in addition to binding effectors or serving as their substrates, operative targets carry a biochemical activity that is modulated by the effector. The perturbation of this activity by the effector leads to effector-triggered susceptibility, an activity often related to immunity (Boller and He, 2009; Dodds and Rathjen, 2010; Win et al., 2012). Clearly NLR-integrated domains must retain the “sensor” activity of the ancestral ET, but they could also retain their biochemical activity, continuing to function in the effector-targeted pathway even as an extraneous domain within a classic NLR architecture. At present, this possibility cannot be discounted given that the biochemical activities of the ancestral ETs and their NLR-integrated counterparts are generally unknown. Additionally, when NLR-fusions occurred recently, there may not have been enough time for the integrated ET to lose its original function and evolve into a decoy. We therefore propose to refer to the extraneous domains of classic NLR proteins described by Cesari et al. (2014) as sensor domains (SD), a term that is agnostic to any potential biochemical activities of the integrated module.
How to test whether or not SDs are decoys? We propose a straightforward genetic test that can reject the decoy hypothesis. Isogenic plants either carrying or lacking the NLR-SD can be challenged with a pathogen strain that lacks the matching avirulence effector (Figure 1). There are several possible outcomes. If the NLR-SD isogenic lines do not differ in their response to the pathogen without the matching effector, the result is inconclusive and the null decoy hypothesis cannot be rejected. If the presence of NLR-SD without the known matching effector shows higher levels of resistance, and there are no signs of typical effector-triggered immunity, then the SD is likely to have retained the ET biochemical activity and contributes to basal immunity in a manner analogous to the ancestral ET. An even more interesting result would be if in the absence of the matching effector, the NLR-SD line is more susceptible as has been shown for several ETs (van Schie and Takken, 2014). In this scenario, another (unrecognized) effector might still be targeting the original biochemical activity of the SD domain. It would be conceptually fascinating if an NLR that functions as a resistance (R) gene against certain strains of a pathogen becomes a susceptibility (S) gene when exposed to other strains. Once again, this concept emphasizes how the outcome of plant-pathogen interactions is so critically dependent on the genotypes of the interacting organisms – a gene that has a certain impact in a particular genetic combination can have the exact opposite effect in another (Jones and Dangl, 2006; van der Hoorn and Kamoun, 2008; Dodds and Rathjen, 2010; Win et al., 2012).
Our goal is not to engage in an exercise in semantics. However, we wish to avoid conceptually restrictive terminology and urge the plant-microbe interactions community to test a rich spectrum of models and hypotheses. The proposed sensor domain terminology would accommodate this breadth of ideas. Ultimately, it may very well turn out that the majority, if not all, of the NLR integrated domains have lost their biochemical activities and have evolved into decoys. Also, it is possible that the sensor domain has already evolved into a decoy prior to recombination into a NLR. Nonetheless, further genetic and biochemical experiments are required to determine whether sensor domains of NLR-SDs are decoys or biochemically functional duplicates of their ancestral ETs.
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