A mechanistic understanding of how plant pathogens modulate their hosts is critical for rationally engineered disease resistance in agricultural systems. Two new studies show that genomically paired plant immune receptors have incorporated decoy domains that structurally mimic pathogen virulence targets to monitor attempted host immunosuppression.
Defense against pathogens in multicellular eukaryotes depends on intracellular immune receptors, yet surveillance by these receptors is poorly understood. Several plant nucleotide-binding, leucine-rich repeat (NB-LRR) immune receptors carry fusions with other protein domains. The Arabidopsis RRS1-R NB-LRR protein carries a C-terminal WRKY DNA binding domain and forms a receptor complex with RPS4, another NB-LRR protein. This complex detects the bacterial effectors AvrRps4 or PopP2 and then activates defense. Both bacterial proteins interact with the RRS1 WRKY domain, and PopP2 acetylates lysines to block DNA binding. PopP2 and AvrRps4 interact with other WRKY domain-containing proteins, suggesting these effectors interfere with WRKY transcription factor-dependent defense, and RPS4/RRS1 has integrated a “decoy” domain that enables detection of effectors that target WRKY proteins. We propose that NB-LRR receptor pairs, one member of which carries an additional protein domain, enable perception of pathogen effectors whose function is to target that domain.
Pathogens play an important part in shaping the structure and dynamics of natural communities, because species are not affected by them equally1, 2. A shared goal of ecology and epidemiology is to predict when a species is most vulnerable to disease. A leading hypothesis asserts that the impact of disease should increase with host abundance, producing a ‘rare-species advantage’3, 4, 5. However, the impact of a pathogen may be decoupled from host abundance, because most pathogens infect more than one species, leading to pathogen spillover onto closely related species6, 7. Here we show that the phylogenetic and ecological structure of the surrounding community can be important predictors of disease pressure. We found that the amount of tissue lost to disease increased with the relative abundance of a species across a grassland plant community, and that this rare-species advantage had an additional phylogenetic component: disease pressure was stronger on species with many close relatives. We used a global model of pathogen sharing as a function of relatedness between hosts, which provided a robust predictor of relative disease pressure at the local scale. In our grassland, the total amount of disease was most accurately explained not by the abundance of the focal host alone, but by the abundance of all species in the community weighted by their phylogenetic distance to the host. Furthermore, the model strongly predicted observed disease pressure for 44 novel host species we introduced experimentally to our study site, providing evidence for a mechanism to explain why phylogenetically rare species are more likely to become invasive when introduced8, 9. Our results demonstrate how the phylogenetic and ecological structure of communities can have a key role in disease dynamics, with implications for the maintenance of biodiversity, biotic resistance against introduced weeds, and the success of managed plants in agriculture and forestry.
Parasite effector proteins target various host cell compartments to alter host processes and promote infection. How effectors cross membrane-rich interfaces to reach these compartments is a major question in effector biology. Growing evidence suggests that effectors use molecular mimicry to subvert host cell machinery for protein sorting. We recently identified CTP1 (chloroplast-targeted protein 1), a candidate effector from the poplar leaf rust fungus Melampsora larici-populina that carries a predicted transit peptide and accumulates in chloroplasts. Here, we show that the CTP1 transit peptide is necessary and sufficient for accumulation in the stroma of chloroplasts, and is cleaved after translocation. CTP1 is part of a Melampsora-specific family of polymorphic secreted proteins whose members translocate and are processed in chloroplasts in a N-terminal signal-dependent manner. Our findings reveal that fungi have evolved effector proteins that mimic plant-specific sorting signals to traffic within plant cells.
Status Summary: Ug99 Lineage – April 2015 - Race TTKSK (Ug99) was the first known race of P. graminis f. sp. tritici with virulence to the stem rust resistance gene Sr31. It also possesses virulence to a wide range of resistance genes of wheat origin, plus others of alien origin. The pathogen is changing rapidly and eleven known variants have been identified within the Ug99 lineage of wheat stem rust. The Ug99 race group is present in 13 countries, with Egypt being the most recent country in which the Ug99 race group was detected (see map).The latest variants are: TTKSF+, detected in South Africa and Zimbabwe from samples collected in 2010 (Pretorius et al. 2012); TTKTT, TTKTK and TTHSK – all collected in Kenya in 2014. All variants are considered to be single step mutations. Acquired virulence to additional important Sr genes, notably Sr24 and Sr36, is known from Kenya (Sr24, Sr36), Eritrea (Sr24), Ethiopia (Sr24, Sr36), Mozambique (Sr24), Rwanda (Sr36), South Africa (Sr24),Tanzania (Sr24, Sr36), Uganda (Sr24, Sr36) and Zimbabwe (Sr24). Race TTKST, carrying combined Sr31 + Sr24 virulence, caused epidemics in Kenya in 2007. Ug99 races carrying combined Sr31 + Sr24 virulence are spreading rapidly throughout Africa and it is considered likely that they will spread further in the future. In addition, virulence to the SrTmp gene has now been acquired by the latest variants detected in Kenya (race TTKTT and race TTKTK).
Attack and counter-attack impose strong reciprocal selection on pathogens and hosts, leading to development of arms race evolutionary dynamics. Here we show that Magnaporthe oryzae avirulence gene AVR-Pik and the cognate rice resistance (R) gene Pik are highly variable, with multiple alleles in which DNA replacements cause amino acid changes. There is tight recognition specificity of the AVR-Pikalleles by the various Pik alleles. We found that AVR-Pik physically binds the N-terminal coiled-coil domain of Pik in a yeast two-hybrid assay as well as in an in planta co-immunoprecipitation assay. This binding specificity correlates with the recognition specificity between AVR and R genes. We propose that AVR-Pik and Pik are locked into arms race co-evolution driven by their direct physical interactions.
Plants sense invasion of potential microbial pathogens using various receptors and launch cascades of innate immune responses that are critical for survival and fecundity. Recognition of pathogens occurs through detection of pathogen-associated patterns (PAMPs) or pathogen effectors, setting off a cascade of signaling events that triggers early cellular and molecular responses. Plant innate immunity is constituted by an elaborate, multilayered system involving two intertwined lines of defense: a first level of immunity termed PAMP–triggered immunity (PTI) or basal resistance, and a second layer of plant defense, mediated by resistance (R) proteins, leading to a complete resistance response often accompanied by the hypersensitive cell death (HR), and called effector-triggered immunity (ETI; Jones & Dangl, 2006). Another form of resistance, that confers partial resistance to pathogens and usually referred as quantitative disease resistance (QDR), has been extensively observed in crops and natural plant populations (Kover & Cheverud, 2007; Poland et al., 2009; Roux et al., 2014). However, there is still very limited information about the molecular mechanisms underlying this form of immunity. More generally, protein kinases play critical roles during immunity in signaling through phosphorylation of target proteins and as modulators of cell metabolism and gene expression (Romeis, 2001; Meng & Zhang, 2013). Pseudokinases are topologically related to protein kinases but lack catalytic residue(s) classically required for phosphotransfer. Interestingly, recent reports identified two Arabidopsis pseudokinases, RKS1 and ZED1, that belong to a gene cluster within the receptor-like cytoplasmic kinase (RLCK)- XII-2 subfamily and confer different forms of immunity.
There is a fungus on our planet which is capable of not one, but two audacious and duplicitous acts: it pretends, on separate occasions, to be a flower and a pollen grain, and its performances are so successful that it manages to fool both the bumblebee and the blueberry bush.
That fungus goes by the tongue-twisting name Monilinia vaccinii-corymbosi, but the common name for the disease it causes is mummy berry (which sounds like it should have its own breakfast cereal). That’s because it has a third act too: turning blueberries into time bombs.
Plant pathogenic fungi are everywhere, as I can attest from the two years I spent studying them in graduate school. They are fascinating specialists evolved to finagle their way into plant bodies and sneak past or exploit plant defense systems with practiced polish.
Some, like the gloriously named rusts, smuts, and bunts, are so specialized that they shuttle between two often wildly unrelated host plant species and can produce up to five types of spores. But M. vacciniii-corymbosi (hereafter M. v-c.) takes this artful and deadly dance to a new level of sophistication and guile with its successful imitation of entire plant organs.
Leaf mold of tomato is caused by the biotrophic fungus Cladosporium fulvum which complies with the gene-for-gene system. The disease was first reported in Japan in the 1920s and has since been frequently observed. Initially only race 0 isolates were reported, but since the consecutive introduction of resistance genes Cf-2, Cf-4, Cf-5 and Cf-9 new races have evolved. Here we first determined the virulence spectrum of 133 C. fulvum isolates collected from 22 prefectures in Japan, and subsequently sequenced the avirulence (Avr) genes Avr2, Avr4, Avr4E, Avr5 and Avr9 to determine the molecular basis of overcoming Cf genes. Twelve races of C. fulvum with a different virulence spectrum were identified, of which races 9, 2.9, 4.9, 4.5.9 and 4.9.11 occur only in Japan. The Avr genes in many of these races contain unique mutations not observed in races identified elsewhere in the world including (i) frameshift mutations and (ii) transposon insertions in Avr2, (iii) point mutations in Avr4 and Avr4E, and (iv) deletions of Avr4E, Avr5 and Avr9. New races have developed by selection pressure imposed by consecutive introductions of Cf-2, Cf-4, Cf-5 and Cf-9 genes in commercially grown tomato cultivars. Our study shows that molecular variations to adapt to different Cf genes in an isolated C. fulvum population in Japan are novel but overall follow similar patterns as those observed in populations from other parts of the world. Implications for breeding of more durable C. fulvumresistant varieties are discussed.
The expression of thein planta-induced geneipiO of the potato late blight pathogenPhytophthora infestanswas analyzed during various developmental stages of its life cycle.ipiO mRNA was detected in zoospores, cysts, germinating cysts, and young mycelia, but not in sporangia or in old mycelia grownin vitro. ipiO is not only expressed in stages prior to infection but also during colonization of potato and tomato leaves. In disease lesions,ipiO mRNA was detected in the water-soaked area and the healthy-looking plant tissue surrounding it. In contrast,ipiO mRNA was not found in necrotized tissue or in sporulating areas of a lesion. To determine more precisely the location and time ofipiO gene expressionin planta,cytological assays were performed using aP. infestanstransformant expressing a transcriptional fusion between theipiO1 promoter and the β-glucuronidase (GUS) reporter gene. GUS staining was found specifically in the subapical and vacuolated area of tips of invading hyphae. The histochemical GUS assays demonstrate thatipiO is expressed during biotrophic stages of the disease cycle.
You are invited to attend a special day on wheat disease resistance at the John Innes Conference Centre on Friday 22 May 2015 in Norwich.
This day will bring together scientists, plant breeders, growers and policy-makers in a series of scientific seminars and networking. The day’s sessions will highlight current research and strategies for delivering increased and sustainable production of wheat in face of the many diseases that infect this crop.
Wheat is the most widely planted crop in the world and has an average production of 650 million tonnes per year, of which 65% is for human consumption. An increasing world population has placed substantial demands on wheat production, a battle exacerbated by the many and emerging diseases which can compromise crop quality and yield.
World-leading scientists from the John Innes Centre, The Genome Analysis Centre (TGAC), and The Sainsbury Laboratory (TSL) are carrying out strategic research into the biology and evolution of wheat diseases, as well as in the genomics and immune responses of wheat. These programmes, which further highlight the integrative and collaborative nature of research across these different institutes on the Norwich Research Park, are required to provide practical solutions to the significant challenge caused by wheat diseases in UK and worldwide.
9:30 Registration and refreshments 10:00 Introduction by John Snape (JIC) 10:10 Dr. Ravi Singh (CIMMYT): Approaches to develop and deliver high yielding, disease resistant wheat germplasm at CIMMYT 10:50 Introduction to the Norwich Rust Group 11:00 Dr. Cristobal Uauy (JIC) 11:25 Refreshments 11:50 Dr. Diane Saunders (TGAC/JIC) 12:15 Prof. James Brown (JIC) 12:40 Lunch 13:40 Dr. Kim Hammond-Kosack (Rothamsted) 14:20 Dr. Brande Wulff (JIC) 14:45 Dr. Matthew Moscou (TSL) 15:10 Refreshments 15:35 Dr. Paul Nicholson (JIC) 16:00 Dr. Ksenia Krasileva (TGAC/TSL) 16:25 Concluding remarks by John Snape (JIC) 16:30 Closing remarks
Microbial pathogens infect host cells by delivering virulence factors (effectors) that interfere with defenses. In plants, intracellular nucleotide-binding/leucine-rich repeat receptors (NLRs) detect specific effector interference and trigger immunity by an unknown mechanism. The Arabidopsis-interacting NLR pair, RRS1-R with RPS4, confers resistance to different pathogens, including Ralstonia solanacearum bacteria expressing the acetyltransferase effector PopP2. We show that PopP2 directly acetylates a key lysine within an additional C-terminal WRKY transcription factor domain of RRS1-R that binds DNA. This disrupts RRS1-R DNA association and activates RPS4-dependent immunity. PopP2 uses the same lysine acetylation strategy to target multiple defense-promoting WRKY transcription factors, causing loss of WRKY-DNA binding and transactivating functions needed for defense gene expression and disease resistance. Thus, RRS1-R integrates an effector target with an NLR complex at the DNA to switch a potent bacterial virulence activity into defense gene activation.
The first layer of plant immunity is activated by cell surface receptor-like kinases (RLKs) and proteins (RLPs) that detect infectious pathogens. Constitutive interaction with the RLK SUPPRESSOR OF BIR1 (SOBIR1) contributes to RLP stability and kinase activity. As RLK activation requires transphosphorylation with a second associated RLK, it remains elusive how RLPs initiate downstream signaling. To address this, we investigated functioning of Cf RLPs that mediate immunity of tomato against Cladosporium fulvum. We employed live-cell imaging and co-immunoprecipitation in tomato and Nicotiana benthamiana to investigate the requirement of associated kinases for Cf activity and ligand-induced subcellular trafficking of Cf-4. Upon elicitation with the matching effector ligands Avr4 and Avr9, BRI1-ASSOCIATED KINASE 1 (BAK1) associates with Cf-4 and Cf-9. Furthermore, Cf-4 that interacts with SOBIR1 at the plasma membrane, is recruited to late endosomes after elicitation. Significantly, BAK1 is required for Avr4-triggered endocytosis, effector-triggered defenses in Cf-4 plants and resistance of tomato against C. fulvum. Our observations indicate that RLP-mediated immune signaling and endocytosis require ligand-induced recruitment of BAK1, reminiscent of BAK1 interaction and subcellular fate of the FLAGELLIN SENSING 2 RLK. This reveals that diverse classes of cell surface immune receptors share common requirements for signaling initiation and endocytosis.
Plant-invading microbes betray their presence to a plant by exposure of antigenic molecules such as small, secreted proteins called ‘effectors’. In Fusarium oxysporum f. sp. lycopersici (Fol) we identified a pair of effector gene candidates, AVR2-SIX5, whose expression is controlled by a shared promoter.
The pathogenicity of AVR2 and SIX5 Fol knockouts was assessed on susceptible and resistant tomato (Solanum lycopersicum) plants carrying I-2. The I-2 NB-LRR protein confers resistance to Fol races carrying AVR2.
Like Avr2, Six5 was found to be required for full virulence on susceptible plants. Unexpectedly, each knockout could breach I-2-mediated disease resistance. So whereas Avr2 is sufficient to induce I-2-mediated cell death, Avr2 and Six5 are both required for resistance. Avr2 and Six5 interact in yeast two-hybrid assays as well as in planta. Six5 and Avr2 accumulate in xylem sap of plants infected with the reciprocal knockouts, showing that lack of I-2 activation is not due to a lack of Avr2 accumulation in the SIX5 mutant.
The effector repertoire of a pathogen determines its host specificity and its ability to manipulate plant immunity. Our findings challenge an oversimplified interpretation of the gene-for-gene model by showing requirement of two fungal genes for immunity conferred by one resistance gene.
All other curves are derived from this basic curve. The arrow indicates that the position of the curve is variable, and depends on the particular host–microorganism interaction. The y-axis denotes host damage as a function of the host response. In this scheme, host damage can occur throughout the host response, but is magnified at both extremes. The host response is represented by a continuum from 'weak' to 'strong'. 'Weak' and 'strong' are terms that can encompass both quantitative and qualitative characteristics of the host response and are used as the best available terms to denote the spectrum of host response as more precise terms are limiting. Weak responses are those that are insufficient, poor or inappropriate — that is, they are not strong enough to benefit the host. Strong responses are those that are excessive, overly robust or inappropriate — that is, they are too strong and can damage the host. When a threshold amount of damage is reached, the host can become symptomatic and if damage is severe, death can ensue. Green, yellow and purple represent health, disease and severe disease, respectively.
Fungal plant pathogens, such as Zymoseptoria tritici (formerly known as Mycosphaerella graminicola), secrete repertoires of effectors to facilitate infection or trigger host defence mechanisms. The discovery and functional characterization of effectors provides valuable knowledge that can contribute to the design of new and effective disease management strategies. Here, we combined bioinformatics approaches with expression profiling during pathogenesis to identify candidate effectors of Z. tritici. In addition, a genetic approach was conducted to map quantitative trait loci (QTLs) carrying putative effectors, enabling the validation of both complementary strategies for effector discovery. In planta expression profiling revealed that candidate effectors were up-regulated in successive waves corresponding to consecutive stages of pathogenesis, contrary to candidates identified by QTL mapping that were, overall, expressed at low levels. Functional analyses of two top candidate effectors (SSP15 and SSP18) showed their dispensability for Z. tritici pathogenesis. These analyses reveal that generally adopted criteria, such as protein size, cysteine residues and expression during pathogenesis, may preclude an unbiased effector discovery. Indeed, genetic mapping of genomic regions involved in specificity render alternative effector candidates that do not match the aforementioned criteria, but should nevertheless be considered as promising new leads for effectors that are crucial for the Z. tritici–wheat pathosystem.
Medicago truncatula is a model legume species used to investigate plant-microorganism interactions, notably root symbioses. Massive population genomic and transcriptomic data now available for this species open the way for a comprehensive investigation of genomic variations associated with adaptation of M. truncatula to its environment. Here we performed a fine-scale genome scan of selective sweep signatures in Medicago truncatula using more than 15 million SNPs identified on 283 accessions from two populations (Circum and Far West), and exploited annotation and published transcriptomic data to identify biological processes associated with molecular adaptation. We identified 58 swept genomic regions with a 15 kb average length and comprising 3.3 gene models on average. The unimodal sweep state probability distribution in these regions enabled us to focus on the best single candidate gene per region. We detected two unambiguous species-wide selective sweeps, one of which appears to underlie morphological adaptation. Population genomic analyses of the remaining 56 sweep signatures indicate that sweeps identified in the Far West population are less population-specific and probably more ancient than those identified in the Circum population. Functional annotation revealed a predominance of immunity-related adaptations in the Circum population. Transcriptomic data from accessions of the Far West population allowed inference of four clusters of co-regulated genes putatively involved in the adaptive control of symbiotic carbon flow and nodule senescence, as well as in other root adaptations upon infection with soil microorganisms. We demonstrate that molecular adaptations in Medicago truncatula were primarily triggered by selective pressures from root-associated micro-organisms.
Yuan Longping High-Tech Agriculture Co Ltd said on Monday that it would stop selling its hybrid rice variety "Liangyou 0293", following a massive crop failure in Anhui province in eastern China, where it was largely cultivated.
"Sales of the 'Liangyou 0293' variety fetched about 7 million yuan ($1.1 million) for the company last year. The latest move is certain to hit profit this year," the listed company, known as Longping High-Tech, said in a regulatory filing.
More than 667 hectares of rice fields in six cities in Anhui province suffered low-yields or even outright crop failure last October due to rice blast, a serious disease caused by the imperfect fungus, according to the provincial seed management station.
Some counties such as Wuhe, one of the rice-producing areas, were hit hard with the yield of rice plummeting to 50 kilograms per mu (0.06 hectare) or to even none, from the expected 500 kilograms.
"I did my best but only a few bags of rice were harvested," said Wang Peijie, a local farmer. "It is almost nothing."
Local farmers said misleading advertisements were to blame for their heavy losses.
On the packages of seeds sold to farmers, the ad claimed the strain had a resistance of 5.6 grades, which indicates an incidence rate of only 25 percent, but inside, a piece of paper showed that the seeds had a resistance of 9 grades, suggesting the possibility of catching a disease is as high as 100 percent, a report from the Guangzhou-based Southern Weekly said.
However, Longping High-Tech said that it was mainly the natural conditions including low temperatures and rains in the rice-growing regions that had led to the rice blast outbreak.
"The variety has been grown in the region for six years, and during the period rice blast had never occurred," according to the statement.
"We are sorry for the losses to farmers ... and insurance companies will take care of that."
Cell death plays a ubiquitous role in plant-microbe interactions, given that it is associated with both susceptible and resistance interactions. A class of cell death-inducing proteins, termed Nep1-like proteins (NLPs), has been reported in bacteria, fungi, and oomycetes. These proteins induce nonspecific necrosis in a variety of dicotyledonous plants. Here, we describe three members of the NLP family from the oomycete Phytophthora infestans (PiNPP1.1, PiNPP1.2, and PiNPP1.3). Using agroinfection with a binary Potato virus X vector, we showed that PiNPP1.1 induces cell death in Nicotiana benthamiana and the host plant tomato. Expression analyses indicated that PiNPP1.1 is up-regulated during late stages of infection of tomato by P. infestans. We compared PiNPP1.1 necrosis-inducing activity to INF1 elicitin, a well-studied protein that triggers the hypersensitive response in Nicotiana spp. Using virus-induced gene silencing, we showed that the cell death induced by PiNPP1.1 is dependent on the ubiquitin ligase-associated protein SGT1 and the heat-shock protein HSP90. In addition, cell death triggered by PiNPP1.1 but not that by INF1 was dependent on the defense-signaling proteins COI1, MEK2, NPR1, and TGA2.2, suggesting distinct signaling requirements. Combined expression of PiNPP1.1 and INF1 in N. benthamiana resulted in enhanced cell death, suggesting synergistic interplay between the two cell-death responses. Altogether, these results point to potentially distinct but interacting cell-death pathways induced by PiNPP1.1 and INF1 in plants.
Hemibiotrophic plant pathogens, such as the oomycete Phytophthora infestans, employ a biphasic infection strategy, initially behaving as biotrophs where minimal symptoms are exhibited by the plant, and subsequently as necrotrophs, feeding on dead plant tissue. The regulation of this transition and the breadth of molecular mechanisms that modulate plant defenses are not well understood, although effector proteins secreted by the pathogen are thought to play a key role. We examined the transcriptional dynamics of P. infestans in a compatible interaction with its host tomato (Solanum lycopersicum), at three infection stages: biotrophy; the transition from biotrophy to necrotrophy; and necrotrophy. The expression data suggested a tight temporal regulation of many pathways associated with suppression of plant defense mechanisms and pathogenicity, including the induction of putative cytoplasmic and apoplastic effectors. Twelve of these were experimentally evaluated to determine their ability to suppress necrosis caused by the P. infestans necrosis-inducing protein PiNPP1.1 in Nicotiana benthamiana. Four effectors suppressed necrosis, suggesting that they might prolong the biotrophic phase. This study suggests that a complex regulation of effector expression modulates the outcome of the interaction.
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