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It has frequently been hypothesized that quantitative resistance increases the durability of qualitative (R-gene mediated) resistance but supporting experimental evidence is rare. To test this hypothesis, near-isogenic lines with/without the R-gene Rlm6 introduced into two Brassica napus cultivars differing in quantitative resistance to Leptosphaeria maculans were used in a 5-yr field experiment. Recurrent selection of natural fungal populations was done annually on each of the four plant genotypes, using crop residues from each genotype to inoculate separately the four series of field trials for five consecutive cropping seasons. Severity of phoma stem canker was measured on each genotype and frequencies of avirulence alleles in L. maculans populations were estimated. Recurrent selection of virulent isolates by Rlm6 in a susceptible background rendered the resistance ineffective by the third cropping season. By contrast, the resistance was still effective after 5 yr of selection by the genotype combining this gene with quantitative resistance. No significant variation in the performance of quantitative resistance alone was noted over the course of the experiment. We conclude that quantitative resistance can increase the durability of Rlm6. We recommend combining quantitative resistance with R-gene mediated resistance to enhance disease control and crop production.

1. Selection during interepidemic stages is crucial for the evolution of pathogen populations. Trade-offs involving aggressiveness (quantitative pathogenicity) have rarely been explored in pathogens with a life cycle requiring the disease-causing organism to change organs within the same host. 2. We investigated the existence of a trade-off between aggressiveness and survival in Phytophthora infestans, the pathogen causing potato late blight. In France, P infestans behaves as an obligate biotroph, surviving in infected tubers. Aggressive isolates, which are favoured during the epidemic, may exhaust their nutrient supply too quickly to bridge seasons, resulting in a possible trade-off between the two life stages. 3. We inoculated tubers with isolates possessing different aggressiveness levels, let them overwinter as outdoor piles at three different sites, and scored the proportion of live tubers the following spring. 4. At two sites, infection caused early tuber sprouting, which can be seen either as a manipulation of the host by the pathogen, or as an attempt by the host to escape. 5. Overwinter survival was higher for control than for inoculated tubers, but did not differ between tubers inoculated with different isolates. This suggests that aggressiveness should gradually increase in P infestans populations, unless a trade-off occurs at another stage of the life cycle.

• Physiological races of the oomycete Albugo candida are biotrophic pathogens of diverse plant species, primarily the Brassicaceae, and cause infections that suppress host immunity to other pathogens. However, A. candida race diversity and the consequences of host immunosuppression are poorly understood in the field. • We report a method that enables sequencing of DNA of plant pathogens and plant-associated microbes directly from field samples (Pathogen Enrichment Sequencing: PenSeq). We apply this method to explore race diversity in A. candida and to detect A. candida-associated microbes in the field (91 A. candida-infected plants). • We show with unprecedented resolution that each host plant species supports colonization by one of 17 distinct phylogenetic lineages, each with an unique repertoire of effector candidate alleles. These data reveal the crucial role of sexual and asexual reproduction, polyploidy and host domestication in A. candida specialization on distinct plant species. Our bait design also enabled phylogenetic assignment of DNA sequences from bacteria and fungi from plants in the field. • This paper shows that targeted sequencing has a great potential for the study of pathogen populations while they are colonizing their hosts. This method could be applied to other microbes, especially to those that cannot be cultured.

In plants, nucleotide-binding domain and leucine-rich repeat (NLR)-containing proteins can form receptor networks to confer hypersensitive cell death and innate immunity. One class of NLRs, known as NLR required for cell death (NRCs), are central nodes in a complex network that protects against multiple pathogens and comprises up to half of the NLRome of solanaceous plants. Given the prevalence of this NLR network, we hypothesised that pathogens convergently evolved to secrete effectors that target NRC activities. To test this, we screened a library of 165 bacterial, oomycete, nematode, and aphid effectors for their capacity to suppress the cell death response triggered by the NRC-dependent disease resistance proteins Prf and Rpi-blb2. Among 5 of the identified suppressors, 1 cyst nematode protein and 1 oomycete protein suppress the activity of autoimmune mutants of NRC2 and NRC3, but not NRC4, indicating that they specifically counteract a subset of NRC proteins independently of their sensor NLR partners. Whereas the cyst nematode effector SPRYSEC15 binds the nucleotide-binding domain of NRC2 and NRC3, the oomycete effector AVRcap1b suppresses the response of these NRCs via the membrane trafficking-associated protein NbTOL9a (Target of Myb 1-like protein 9a). We conclude that plant pathogens have evolved to counteract central nodes of the NRC immune receptor network through different mechanisms. Coevolution with pathogen effectors may have driven NRC diversification into functionally redundant nodes in a massively expanded NLR network.

Infection-phase–specific expression of putative effectors has been demonstrated by transcriptomic time-course experiments, among others, in the obligate biotrophic poplar leaf rust Melampsora larici-populina [7]; the hemibiotrophic fungus Colletotrichum higginsianum, which causes anthracnose during Arabidopsis thaliana infection [8]; the obligate biotrophic barley fungus Blumeria graminis [9]; the root mutualistic fungus Serendipita indica (former Piriformospora indica) [5]; and the maize-infecting biotroph U. maydis [10]. Different modes of action (self-binding and self-modifying, activating or inhibiting activities) of effectors described in the text may be applied to serve the listed strategies (text on grey oval background). https://doi.org/10.1371/journal.ppat.1006992.g001 The self-binder and self-modifier Effectors with a defensive mode of action either sequester potential microbe-associated molecular patterns (MAMPs) or modify their cell walls upon penetration to minimize recognition. Other effectors show a high degree of specificity even when they target members of expanded protein families, as is the case for the M. oryzae effector Avr-Pii, which targets specific vesicle-tethering Exo70 subunits involved in host immune responses, or the P. infestans effector PexRD54, which targets a specific autophagy-modulating ubiquitin-like ATG8 family member [46, 47]. [...]sensor domains fused to NLRs might serve as an informative way to preselect common effector targets [53].

Plants are exposed to a wide range of potential pathogens, which derive from diverse phyla. Therefore, plants have developed successful defense mechanisms during co-evolution with different pathogens. Besides many specialized defense mechanisms, the plant cell wall represents a first line of defense. It is actively reinforced through the deposition of cell wall appositions, so-called papillae, at sites of interaction with intruding microbial pathogens. The papilla is a complex structure that is formed between the plasma membrane and the inside of the plant cell wall. Even though the specific biochemical composition of papillae can vary between different plant species, some classes of compounds are commonly found which include phenolics, reactive oxygen species, cell wall proteins, and cell wall polymers. Among these polymers, the (1,3)-β-glucan callose is one of the most abundant and ubiquitous components. Whereas the function of most compounds could be directly linked with cell wall reinforcement or an anti-microbial effect, the role of callose has remained unclear. An evaluation of recent studies revealed that the timing of the different papilla-forming transport processes is a key factor for successful plant defense.

Interactions between plant pathogens and their hosts are highly dynamic and mainly driven by pathogen effectors and plant receptors. Host-pathogen co-evolution can cause rapid diversification or loss of pathogen genes encoding host-exposed proteins. The molecular mechanisms that underpin such sequence dynamics remains poorly investigated at the scale of entire pathogen species. Here, we focus on AvrStb6 , a major effector of the global wheat pathogen Zymoseptoria tritici , evolving in response to the cognate receptor Stb6 , a resistance widely deployed in wheat. We comprehensively captured effector gene evolution by analyzing a global thousand-genome panel using reference-free sequence analyses. We found that AvrStb6 has diversified into 59 protein isoforms with a strong association to the pathogen spreading to new continents. Across Europe, we found the strongest differentiation of the effector consistent with high rates of Stb6 deployment. The AvrStb6 locus showed also a remarkable diversification in transposable element content with specific expansion patterns across the globe. We detected AvrStb6 gene losses and evidence for transposable element-mediated disruptions. We used virulence datasets of genome-wide association mapping studies to predict virulence changes across the global panel. Genomic predictions suggested marked increases in virulence on Stb6 cultivars concomitant with the spread of the pathogen to Europe and the subsequent spread to further continents. Finally, we genotyped French bread wheat cultivars for Stb6 and monitored resistant cultivar deployment concomitant with AvrStb6 evolution. Taken together, our data provides a comprehensive view of how a rapidly diversifying effector locus can undergo large-scale sequence changes concomitant with gains in virulence on resistant cultivars. The analyses highlight also the need for large-scale pathogen sequencing panels to assess the durability of resistance genes and improve the sustainability of deployment strategies.

Plant phenotype is a complex entity largely controlled by the genotype and various environmental factors. Importantly, co-evolution has allowed plants to coexist with the biotic factors in their surroundings. Recently, plant endophytes as an external plant phenotype, forming part of the complex plethora of the plant microbial assemblage, have gained immense attention from plant scientists. Functionally, endophytes impact the plant in many ways, including increasing nutrient availability, enhancing the ability of plants to cope with both abiotic and biotic stress, and enhancing the accumulation of important plant secondary metabolites. The current state of research has been devoted to evaluating the phenotypic impacts of endophytes on host plants, including their direct influence on plant metabolite accumulation and stress response. However, there is a knowledge gap in how genetic factors influence the interaction of endophytes with host plants, pathogens, and other plant microbial communities, eventually controlling the extended microbial plant phenotype. This review will summarize how host genetic factors can impact the abundance and functional diversity of the endophytic microbial community, how endophytes influence host gene expression, and the host–endophyte–pathogen disease triangle. This information will provide novel insights into how breeders could specifically target the plant–endophyte extended phenotype for crop improvement.

Background The colocalization of two resistance ( R ) genes on chromosome 13 of soybean ( Glycine max (L.) Merrill) that confer resistance against the soybean aphid ( Aphis glycines ) and soybean mosaic virus (SMV) gives rise to a very unique R-avr tritrophic incompatible interaction system that goes across biological kingdoms. In this tritrophic system, the insect is the only natural vector of the virus and soybean is a host-plant for both pests/pathogen. The almost unavoidable co-evolution of pathogen-vector with that of the R -genes in soybean plants through an endless arms race to avoid each other’s defense-attack mechanisms raises interesting questions. The objectives of this work were to ( i ) develop double-resistant recombinant inbred lines (RILs) with a Rag2-Rsv1-h gene haplotype in coupling phase using resistance alleles from two different genetic sources (PI 243540 (Rag2) and Suweon 97 (Rsv1-h) ), ( ii ) confirm phenotypically the resistant reaction against both pests in double-resistant RILs, and ( iii ) dissect the Rag2-Rsv1-h region with molecular markers and investigate the potential for structural variation. Results We observed a recombination event in identified double-resistant F 3:5 RILs in a region of chromosome 13 ca. 21 kb long (between positions 30,297,227 and 30,318,949 in Wm82.a2.v1) that lies between the reported locations of the Rsv1-h and Rag2 genes (29,815,463--29,912,369 and 30,412,581--30,466,533 intervals, respectively, based on Wm82.a2.v1), indicating the double-resistant haplotype is in coupling phase. The tight LD estimates obtained between haplotype markers underscored the physical proximity of the two resistance genes. Only 10 recombinant haplotype classes (excluding double heterozygotes) were observed among the 51 that were possible with a four loci haplotype. The 10 recombinant classes represented 15 out of 192 screened individuals. A joint SMV-aphid phenotypic greenhouse screen allowed us to identify the best aphid biotype 1 and SMV-G1, double resistant haplotype class in recombinant progeny. Our molecular marker results agree with previous fine-mapping reports and preclude the presence of resistance genes other than Rag2 and Rsv1-h in double-resistant RILs. A comparative genomic hybridization analysis revealed no obvious structural variants in the region. Conclusions To our knowledge, this is the first report of double-resistant Rag2-Rsv1-h soybean RILs that used a plant-insect-pathogen tritrophic system for germplasm enhancement. The co-occurrence of Rag and Rsv genes in a region that clusters resistance genes on chromosome 13 may be a unique feature of domesticated soybean. The recombinant genotypes will be useful in breeding to develop soybean cultivars with resistance to both the vector and the virus. The parental and recombinant genotypes may be helpful in future studies to elucidate interesting evolutionary questions regarding vector, host, and virus tritrophic systems.

Plants are continuously threatened by pathogen attack and, as such, they have evolved mechanisms to evade, escape and defend themselves against pathogens. However, it is not known what types of defense mechanisms a plant would already possess to defend against a potential pathogen that has not co-evolved with the plant. We addressed this important question in a comprehensive manner by studying the responses of 1041 accessions of Arabidopsis thaliana to the foliar pathogen Pseudomonas syringae pv. tomato (Pst) DC3000. We characterized the interaction using a variety of established methods, including different inoculation techniques, bacterial mutant strains, and assays for the hypersensitive response, salicylic acid (SA) accumulation and reactive oxygen species production. Fourteen accessions showed resistance to infection by Pst DC3000. Of these, two accessions had a surface-based mechanism of resistance, six showed a hypersensitive-like response while three had elevated SA levels. Interestingly, A. thaliana was discovered to have a recognition system for the effector AvrPto, and HopAM1 was found to modulate Pst DC3000 resistance in two accessions. Our comprehensive study has significant implications for the understanding of natural disease resistance mechanisms at the species level and for the ecology and evolution of plant–pathogen interactions.