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Multicellular organisms activate immunity upon recognition of pathogen-associated molecular patterns (PAMPs). Chitin is the major component of fungal cell walls, and chitin oligosaccharides act as PAMPs in plant and mammalian cells. Microbial pathogens deliver effector proteins to suppress PAMP-triggered host immunity and to establish infection. Here, we show that the LysM domain-containing effector protein Ecp6 of the fungal plant pathogen Cladosporium fulvum mediates virulence through perturbation of chitin-triggered host immunity. During infection, Ecp6 sequesters chitin oligosaccharides that are released from the cell walls of invading hyphae to prevent elicitation of host immunity. This may represent a common strategy of host immune suppression by fungal pathogens, because LysM effectors are widely conserved in the fungal kingdom.

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 SUPPRESSOR OF BIR1 (SOBIR1) RLK 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. We employed live‐cell imaging, gene silencing and coimmunoprecipitation to investigate the requirement of associated kinases for functioning and ligand‐induced subcellular trafficking of Cf RLPs that mediate immunity of tomato against Cladosporium fulvum. Our research shows that after elicitation with matching effector ligands Avr4 and Avr9, BRI1‐ASSOCIATED KINASE 1/SOMATIC EMBRYOGENESIS RECEPTOR KINASE 3 (BAK1/SERK3) associates with Cf‐4 and Cf‐9. BAK1/SERK3 is required for the effector‐triggered hypersensitive response and resistance of tomato against C. fulvum. Furthermore, Cf‐4 interacts with SOBIR1 at the plasma membrane and is recruited to late endosomes upon Avr4 trigger, also depending on BAK1/SERK3. These observations indicate that RLP‐mediated resistance and endocytosis require ligand‐induced recruitment of BAK1/SERK3, reminiscent of BAK1/SERK3 interaction and subcellular fate of the FLAGELLIN SENSING 2 (FLS2) RLK. This reveals that diverse classes of cell surface immune receptors share common requirements for initiation of resistance and endocytosis.

Biotrophic fungi are one group of heterogeneous organisms and these fungi differ in their traits like mode of nutrition, types of reproduction, and dispersal systems. Generally, based on the nutritional mode, fungi are classified into three broad categories, viz. biotrophs, necrotrophs, and hemi-biotrophs. Biotrophs derive their nutrients and energy from living plant cells and survive within the interstitial space of the cells. Biotrophic fungi cause serious crop diseases but are highly challenging to investigate and develop a treatment strategy. Blumeria (Erysiphe) graminis, Uromyces fabae, Ustilago maydis, Cladosporium fulvum, Puccinia graminis, and Phytophthora infestans are some of the significant biotrophic fungi that affect mainly plants. One among the biotrophic fungus, Pneumocystis jirovecii (Taphrinomycotina subphylum of the Ascomycota) exclusively a human pathogen, can cause lung diseases such as “pneumocystis.” Biotrophic fungus widely parasitizing Solanaceae family crops (Tomato and potato) has done massive damage to the crops and has led to economic impact worldwide. During infection and for nutrient absorption, biotrophs develops external appendages such as appressoria or haustoria. The hyphae or appressorium adheres to the plant cell wall and collapses the layers for their nutrient absorption. The pathogen also secretes effector molecules to escape from the plant defense mechanism. Later, plants activate their primary and secondary defense mechanisms; however, the pathogen induces virulence genes to escape the host immune responses. Obligate biotrophic fungi pathogenicity has not been fully understood at the molecular level because of the complex interaction, recognition, and signaling with the host. This review summarizes the mechanism of infection in the host, and immune response to emphasize the understanding of the biotrophic fungal biology and pathogenesis in crops. Thus, the detailed review will pave the way to design methods to overcome the resistance of biotrophic fungi and develop disease-free crops.

Tomato leaf mold caused by Passalora fulva was found on two tomato varieties carrying the Cf-9 gene in Japan, in 2007. The isolates obtained from Chiba and Fukushima were identified as race 4.9.11, and those from Gunma were races 4.9 or 4.9.11. This is the first report in Japan of tomato leaf mold caused by P. fulva strains that can overcome the Cf-9 gene.

Plants lack the seemingly unlimited receptor diversity of a somatic adaptive immune system as found in vertebrates and rely on only a relatively small set of innate immune receptors to resist a myriad of pathogens. Here, we show that disease-resistant tomato plants use an efficient mechanism to leverage the limited nonself recognition capacity of their innate immune system. We found that the extracellular plant immune receptor protein Cf-2 of the red currant tomato (Solanum pimpinellifolium) has acquired dual resistance specificity by sensing perturbations in a common virulence target of two independently evolved effectors of a fungus and a nematode. The Cf-2 protein, originally identified as a monospecific immune receptor for the leaf mold fungus Cladosporium fulvum , also mediates disease resistance to the root parasitic nematode Globodera rostochiensis pathotype Ro1-Mierenbos. The Cf-2–mediated dual resistance is triggered by effector-induced perturbations of the apoplastic Rcr3 ᵖⁱᵐ protein of S. pimpinellifolium . Binding of the venom allergen-like effector protein Gr-VAP1 of G. rostochiensis to Rcr3 ᵖⁱᵐ perturbs the active site of this papain-like cysteine protease. In the absence of the Cf-2 receptor, Rcr3 ᵖⁱᵐ increases the susceptibility of tomato plants to G. rostochiensis , thus showing its role as a virulence target of these nematodes. Furthermore, both nematode infection and transient expression of Gr-VAP1 in tomato plants harboring Cf-2 and Rcr3 ᵖⁱᵐ trigger a defense-related programmed cell death in plant cells. Our data demonstrate that monitoring host proteins targeted by multiple pathogens broadens the spectrum of disease resistances mediated by single plant immune receptors.

Summary Leucine‐rich repeat‐receptor‐like proteins (LRR‐RLPs) and LRR‐receptor‐like kinases (LRR‐RLKs) trigger immune signalling to promote plant resistance against pathogens. LRR‐RLPs lack an intracellular kinase domain, and several of these receptors have been shown to constitutively interact with the LRR‐RLK Suppressor of BIR1‐1/EVERSHED (SOBIR1/EVR) to form signalling‐competent receptor complexes. Ligand perception by LRR‐RLPs initiates recruitment of the co‐receptor BRI1‐Associated Kinase 1/Somatic Embryogenesis Receptor Kinase 3 (BAK1/SERK3) to the LRR‐RLP/SOBIR1 complex, thereby activating LRR‐RLP‐mediated immunity. We employed phosphorylation analysis of in planta‐produced proteins, live cell imaging, gene silencing and co‐immunoprecipitation to investigate the roles of SOBIR1 and BAK1 in immune signalling. We show that Arabidopsis thaliana (At) SOBIR1, which constitutively activates immune responses when overexpressed in planta, is highly phosphorylated. Moreover, in addition to the kinase activity of SOBIR1 itself, kinase‐active BAK1 is essential for AtSOBIR1‐induced constitutive immunity and for the phosphorylation of AtSOBIR1. Furthermore, the defence response triggered by the tomato LRR‐RLP Cf‐4 on perception of Avr4 from the extracellular pathogenic fungus Cladosporium fulvum is dependent on kinase‐active BAK1. We argue that, in addition to the trans‐autophosphorylation of SOBIR1, it is likely that SOBIR1 and BAK1 transphosphorylate, and thereby activate the receptor complex. The signalling‐competent cell surface receptor complex subsequently activates downstream cytoplasmic signalling partners to initiate RLP‐mediated immunity.

The plant immune system is activated by microbial patterns that are detected as nonself molecules. Such patterns are recognized by immune receptors that are cytoplasmic or localized at the plasma membrane. Cell surface receptors are represented by receptor-like kinases (RLKs) that frequently contain extracellular leucine-rich repeats and an intracellular kinase domain for activation of downstream signaling, as well as receptor-like proteins (RLPs) that lack this signaling domain. It is therefore hypothesized that RLKs are required for RLPs to activate downstream signaling. The RLPs Cf-4 and Ve1 of tomato (Solanum lycopersicum) mediate resistance to the fungal pathogens Cladosporium fulvum and Verticillium dahliae , respectively. Despite their importance, the mechanism by which these immune receptors mediate downstream signaling upon recognition of their matching ligand, Avr4 and Ave1, remained enigmatic. Here we show that the tomato ortholog of the Arabidopsis thaliana RLK Suppressor Of BIR1-1/Evershed (SOBIR1/EVR) and its close homolog S. lycopersicum (Sl)SOBIR1-like interact in planta with both Cf-4 and Ve1 and are required for the Cf-4– and Ve1-mediated hypersensitive response and immunity. Tomato SOBIR1/EVR interacts with most of the tested RLPs, but not with the RLKs FLS2, SERK1, SERK3a, BAK1, and CLV1. SOBIR1/EVR is required for stability of the Cf-4 and Ve1 receptors, supporting our observation that these RLPs are present in a complex with SOBIR1/EVR in planta . We show that SOBIR1/EVR is essential for RLP-mediated immunity and propose that the protein functions as a regulatory RLK of this type of cell-surface receptors.

Current models of plant-pathogen interactions stipulate that pathogens secrete effector proteins that disable plant defense components known as virulence targets. Occasionally, the perturbations caused by these effectors trigger innate immunity via plant disease resistance proteins as described by the \"guard hypothesis.\" This model is nicely illustrated by the interaction between the fungal plant pathogen Cladosporium fulvum and tomato. C. fulvum secretes a protease inhibitor Avr2 that targets the tomato cysteine protease Rcr3pim. In plants that carry the resistance protein Cf2, Rcr3pim is required for resistance to C. fulvum strains expressing Avr2, thus fulfilling one of the predictions of the guard hypothesis. Another prediction of the guard hypothesis has not yet been tested. Considering that virulence targets are important components of defense, different effectors from unrelated pathogens are expected to evolve to disable the same host target. In this study we confirm this prediction using a different pathogen of tomato, the oomycete Phytophthora infestans that is distantly related to fungi such as C. fulvum. This pathogen secretes an array of protease inhibitors including EPIC1 and EPIC2B that inhibit tomato cysteine proteases. Here we show that, similar to Avr2, EPIC1 and EPIC2B bind and inhibit Rcr3pim. However, unlike Avr2, EPIC1 and EPIC2B do not trigger hypersensitive cell death or defenses on Cf-2/Rcr3pim tomato. We also found that the rcr3-3 mutant of tomato that carries a premature stop codon in the Rcr3 gene exhibits enhanced susceptibility to P. infestans, suggesting a role for Rcr3pim in defense. In conclusion, our findings fulfill a key prediction of the guard hypothesis and suggest that the effectors Avr2, EPIC1, and EPIC2B secreted by two unrelated pathogens of tomato target the same defense protease Rcr3pim. In contrast to C. fulvum, P. infestans appears to have evolved stealthy effectors that carry inhibitory activity without triggering plant innate immunity.

Background Leaf mold, one of the major diseases of tomato caused by Cladosporium fulvum ( C. fulvum ), can dramatically reduce the yield and cause multimillion dollar losses annually worldwide. Mapping the resistance genes ( R genes) of C. fulvum and devising MAS based strategies for breeding new cultivars is an effective approach to improve the resistance in tomato. Up to now, many C. fulvum genes or QTLs have been mapped using different genetic materials, but few studies focused on Cf -10 gene positioning. Results In this study, we investigated the genetic rules for Cf -10 and used a novel combinatorial strategy to rapidly map the Cf -10 gene. Initially, the performance of F 1 , F 2 and BC 1 F 1 individuals after infection, demonstrated that the resistance against C. fulvum was controlled by a single dominant gene. Two pools of resistant and susceptible individuals from F 2 population were investigated, using mapping by sequencing approach and Cf -10 was found to be localized to 3.35 Mb and 3.74 Mb on chromosome 1, employing SNP/InDel index methods, respectively. After accounting for overlapping regions, these two algorithms yielded a total length of 3.29 Mb, narrowing down the target region. We further developed five serviceable KASP markers for this region based on sequencing data and conducted local QTL mapping using individuals from the F 2 population, except for mapping by sequencing as mentioned above. Finally Cf -10 gene was mapped spanning a region of 790 kb, where only one gene ( Solyc01g007130.3 ) was annotated as probable receptor protein kinase TMK1 with a LRR motif, a common R gene characteristic. The RT-qPCR analysis further confirmed the localization and the relative expression of Solyc01g007130.3 in Ontario 792 and was found to be significantly higher than that in Moneymaker at 9 dpi and 12 dpi, respectively. Conclusion This study proposed a novel combinatorial strategy by combining SNP-index, InDel-index analyses and local QTL mapping using KASP genotyping approach to rapidly map genes responsible for specific traits and provided a robust base for cloning the Cf -10 gene. Furthermore, these analyses suggest that Solyc01g007130.3 is a potential candidate to be regarded as Cf -10 gene.

Secreted effector proteins enable plant pathogenic fungi to manipulate host defenses for successful infection. Mycosphaerella graminicola causes Septoria tritici blotch disease of wheat (Triticum aestivum) leaves. Leaf infection involves a long (approximately 7 d) period of symptomless intercellular colonization prior to the appearance of necrotic disease lesions. Therefore, M. graminicola is considered as a hemibiotrophic (or necrotrophic) pathogen. Here, we describe the molecular and functional characterization of M. graminicola homologs of (for extracellular protein 6), the Lysin (LysM) domain-containing effector from the biotrophic tomato (Solanum lycopersicum) leaf mold fungus Cladosporiumfulvum, which interferes with chitin-triggered immunity in plants. Three LysM effector homologs are present in the M. graminicola genome, referred to as Mg3LysM, Mg1LysM, and MgxLysM, Mg3LysM and Mg1LysM genes were strongly transcriptionally up-regulated specifically during symptomless leaf infection. Both proteins bind chitin; however, only Mg3LysM blocked the elicitation of chitin-induced plant defenses. In contrast to C. fulvum Ecp6, both Mg1LysM and Mg3LysM also protected fungal hyphae against plant-derived hydrolytic enzymes, and both genes show significantly more nucleotide polymorphism giving rise to nonsynonymous amino acid changes. While Mg1LysM deletion mutant strains of M. graminicola were fully pathogenic toward wheat leaves, Mg3LysM mutant strains were severely impaired in leaf colonization, did not trigger lesion formation, and were unable to undergo asexual sporulation. This virulence defect correlated with more rapid and pronounced expression of wheat defense genes during the symptomless phase of leaf colonization. These data highlight different functions for MgLysM effector homologs during plant infection, including novel activities that distinguish these proteins from C. fulvum Ecp6.