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Background The annual yield losses caused by the Rice Blast Fungus, Magnaporthe oryzae , range to the equivalent for feeding 60 million people. To ward off infection by this fungus, rice has evolved a generic basal immunity (so called compatible interaction), which acts in concert with strain-specific defence (so-called incompatible interaction). The plant-defence hormone jasmonic acid (JA) promotes the resistance to M. oryzae , but the underlying mechanisms remain elusive. To get more insight into this open question, we employ the JA-deficient mutants, cpm2 and hebiba , and dissect the JA-dependent defence signalling in rice for both, compatible and incompatible interactions. Results We observe that both JA-deficient mutants are more susceptible to M. oryzae as compared to their wild-type background, which holds true for both types of interactions as verified by cytological staining. Secondly, we observe that transcripts for JA biosynthesis ( OsAOS2 and OsOPR7 ), JA signalling ( OsJAZ8 , OsJAZ9 , OsJAZ11 and OsJAZ13 ), JA-dependent phytoalexin synthesis ( OsNOMT ), and JA-regulated defence-related genes, such as OsBBTI2 and OsPR1a , accumulate after fungal infection in a pattern that correlates with the amplitude of resistance. Thirdly, induction of defence transcripts is weaker during compatible interaction. Conclusion The study demonstrates the pivotal role of JA in basal immunity of rice in the resistance to M. oryzae in both, compatible and incompatible interactions.

Late blight, caused by Phytophthora infestans ( P. infestans ), is a devastating plant disease. P. infestans genome encodes hundreds of effectors, complicating the interaction between the pathogen and its host and making it difficult to understand the interaction mechanisms. In this study, the late blight-resistant potato cultivar Ziyun No.1 and the susceptible potato cultivar Favorita were infected with P. infestans isolate SCPZ16-3-1 to investigate the global expression profiles during the compatible and incompatible interactions using dual RNA sequencing (RNA-seq). Most of the expressed Arg-X-Leu-Arg (RXLR) effector genes were suppressed during the first 24 h of infection, but upregulated after 24 h. Moreover, P. infestans induced more specifically expressed genes (SEGs), including RXLR effectors and cell wall-degrading enzymes (CWDEs)-encoding genes, in the compatible interaction. The resistant potato activated a set of biotic stimulus responses and phenylpropanoid biosynthesis SEGs, including kirola-like protein, nucleotide-binding site-leucine-rich repeat (NBS-LRR), disease resistance, and kinase genes. Conversely, the susceptible potato cultivar upregulated more kinase, pathogenesis-related genes than the resistant cultivar. This study is the first study to characterize the compatible and incompatible interactions between P. infestans and different potato cultivars and provides the genome-wide expression profiles for RXLR effector, CWDEs, NBS-LRR protein, and kinase-encoding genes.

Tomato (S olanum lycopersicum ) cv. Moneymaker (MM) is very susceptible to the grey mould Botrytis cinerea , while quantitative resistance in the wild species Solanum habrochaites (accession LYC4) has been reported. In leaf inoculation assays, an effect of nutrient and spore concentration on disease incidence was observed. Resistance in LYC4 leaves was manifested as a high incidence of tiny black, dispersed spots which did not expand (“incompatible interaction”) and was pronounced when B. cinerea was inoculated at high spore density (1000 spores/µL) in medium with 10 mM sucrose and 10 mM phosphate buffer. Under the same condition, a high frequency of expanding lesions was observed on MM leaves (“compatible interaction”). Remarkably, inoculation of LYC4 with a high spore density in medium with higher concentrations of sucrose and/or phosphate as well as lower spore density (30 spores/µL) in medium with low sucrose and phosphate, all resulted in a higher percentage of expanding lesions. The lesion sizes at 3 days post inoculation differed markedly between all these inoculation conditions. This inoculation method provides a convenient tool to study mechanisms that determine the distinction between compatible and incompatible interactions between B. cinerea and a host plant.

Background Bacterial blight, which is caused by Xanthomonas oryzae pv. oryzae ( Xoo ), is a devastating rice disease worldwide. Rice introgression line H471, derived from the recurrent parent Huang-Hua-Zhan (HHZ) and the donor parent PSBRC28, exhibits broad-spectrum resistance to Xoo , including to the highly virulent Xoo strain PXO99 A , whereas its parents are susceptible to PXO99 A . To characterize the responses to Xoo , we compared the proteome profiles of the host and pathogen in the incompatible interaction (H471 inoculated with PXO99 A ) and the compatible interaction (HHZ inoculated with PXO99 A ). Results In this study, a total of 374 rice differentially abundant proteins (DAPs) and 117 Xoo DAPs were detected in the comparison between H471 + PXO99 A and HHZ + PXO99 A . Most of the Xoo DAPs related to pathogen virulence, including the outer member proteins, type III secretion system proteins, TonB-dependent receptors, and transcription activator-like effectors, were less abundant in the incompatible interaction than in the compatible interaction. The rice DAPs were mainly involved in secondary metabolic processes, including phenylalanine metabolism and the biosynthesis of flavonoids and phenylpropanoids. Additionally, some DAPs involved in the phenolic phytoalexin and salicylic acid (SA) biosynthetic pathways accumulated much more in H471 than in HHZ after the inoculation with PXO99 A , suggesting that phytoalexin and SA productions were induced faster in H471 than in HHZ. Further analyses revealed that the SA content increased much more rapidly in H471 than in HHZ after the inoculation, suggesting that the SA signaling pathway was activated faster in the incompatible interaction than in the compatible interaction. Conclusions Overall, our results indicate that during an incompatible interaction between H471 and PXO99 A , rice plants prevent pathogen invasion and also initiate multi-component defense responses that inhibit disease development.

Meloidogyne graminicola is a widely spread nematode pest of rice that reduces crop yield up to 20% on average in Asia, with devastating consequences for local and global rice production. Due to the ban on many chemical nematicides and the recent changes in water management practices in rice agriculture, an even greater impact of M. graminicola can be expected in the future, stressing the demand for the development of new sustainable nematode management solutions. Recently, a source of resistance to M. graminicola was identified in the Oryza sativa japonica rice variety Zhonghua 11 (Zh11). In the present study, we examine the genetics of the Zh11 resistance to M. graminicola and provide new insights into its cellular and molecular mechanisms. The segregation of the resistance in F 2 hybrid populations indicated that two dominant genes may be contributing to the resistance. The incompatible interaction of M. graminicola in Zh11 was distinguished by a lack of swelling of the root tips normally observed in compatible interactions. At the cellular level, the incompatible interaction was characterised by a rapid accumulation of reactive oxygen species in the vicinity of the nematodes, accompanied by extensive necrosis of neighbouring cells. The expression profiles of several genes involved in plant immunity were analysed at the early stages of infection during compatible (susceptible plant) and incompatible (resistant plant) interactions. Notably, the expression of OsAtg4 and OsAtg7 , significantly increased in roots of resistant plants in parallel with the cell death response, suggesting that autophagy is activated and may contribute to the resistance-mediated hypersensitive response. Similarly, transcriptional regulation of genes involved in hormonal pathways in Zh11 indicated that salicylate signalling may be important in the resistance response towards M. graminicola . Finally, the nature of the resistance to M. graminicola and the potential exploitation of the Zh11 resistance for breeding are discussed.

The Hessian fly is a destructive pest of wheat. Employing additional molecular strategies can complement wheat’s native insect resistance. However, this requires functional characterization of Hessian-fly-responsive genes, which is challenging because of wheat genome complexity. The diploid Brachypodium distachyon (Bd) exhibits nonhost resistance to Hessian fly and displays phenotypic/molecular responses intermediate between resistant and susceptible host wheat, offering a surrogate genome for gene characterization. Here, we compared the transcriptomes of Biotype L larvae residing on resistant/susceptible wheat, and nonhost Bd plants. Larvae from susceptible wheat and nonhost Bd plants revealed similar molecular responses that were distinct from avirulent larval responses on resistant wheat. Secreted salivary gland proteins were strongly up-regulated in all larvae. Genes from various biological pathways and molecular processes were up-regulated in larvae from both susceptible wheat and nonhost Bd plants. However, Bd larval expression levels were intermediate between larvae from susceptible and resistant wheat. Most genes were down-regulated or unchanged in avirulent larvae, correlating with their inability to establish feeding sites and dying within 4–5 days after egg-hatch. Decreased gene expression in Bd larvae, compared to ones on susceptible wheat, potentially led to developmentally delayed 2nd-instars, followed by eventually succumbing to nonhost resistance defense mechanisms.

Key message Reactive oxygen species (ROS) oxidize methionine to methionine sulfoxide (MetSO) and thereby inactivate proteins. Methionine sulfoxide reductase (MSR) enzyme converts MetSO back to the reduced form and thereby detoxifies the effect of ROS. Our results show that Arabidopsis thaliana MSR enzyme coding gene MSRB8 is required for effector-triggered immunity and containment of stress-induced cell death in Arabidopsis. Plants activate pattern-triggered immunity (PTI), a basal defense, upon recognition of evolutionary conserved molecular patterns present in the pathogens. Pathogens release effector molecules to suppress PTI. Recognition of certain effector molecules activates a strong defense, known as effector-triggered immunity (ETI). ETI induces high-level accumulation of reactive oxygen species (ROS) and hypersensitive response (HR), a rapid programmed death of infected cells. ROS oxidize methionine to methionine sulfoxide (MetSO), rendering several proteins nonfunctional. The methionine sulfoxide reductase (MSR) enzyme converts MetSO back to the reduced form and thereby detoxifies the effect of ROS. Though a few plant MSR genes are known to provide tolerance against oxidative stress, their role in plant–pathogen interaction is not known. We report here that activation of cell death by avirulent pathogen or UV treatment induces expression of MSRB7 and MSRB8 genes. The T-DNA insertion mutant of MSRB8 exaggerates HR-associated and UV-induced cell death and accumulates a higher level of ROS than wild-type plants. The negative regulatory role of MSRB8 in HR is further supported by amiRNA and overexpression lines. Mutants and overexpression lines of MSRB8 are susceptible and resistant respectively, compared to the wild-type plants, against avirulent strains of Pseudomonas syringae pv. tomato DC3000 ( Pst ) carrying AvrRpt2 , AvrB , or AvrPphB genes. However, the MSRB8 gene does not influence resistance against virulent Pst or P. syringae pv. maculicola ( Psm ) pathogens. Our results altogether suggest that MSRB8 function is required for ETI and containment of stress-induced cell death in Arabidopsis .

BACKGROUND AND AIMS: Sclerotinia sclerotiorum can attack >400 plant species worldwide. Very few studies have investigated host-pathogen interactions at the plant surface and cellular level in resistant genotypes of oilseed rape/canola (Brassica napus). METHODS: Infection processes of S. sclerotiorum were examined on two B. napus genotypes, one resistant cultivar 'Charlton' and one susceptible 'RQ001-02M2' by light and scanning electron microscopy from 2 h to 8 d post-inoculation (dpi). KEY RESULTS: The resistant 'Charlton' impeded fungal growth at 1, 2 and 3 dpi, suppressed formation of appresoria and infection cushions, caused extrusion of protoplast from hyphal cells and produced a hypersensitive reaction. At 8 dpi, whilst in 'Charlton' pathogen invasion was mainly confined to the upper epidermis, in the susceptible 'RQ001-02M2', colonization up to the spongy mesophyll cells was evident. Calcium oxalate crystals were found in the upper epidermis and in palisade cells in susceptible 'RQ001-02M2' at 6 dpi, and throughout leaf tissues at 8 dpi. In resistant 'Charlton', crystals were not observed at 6 dpi, whereas at 8 dpi they were mainly confined to the upper epidermis. Starch deposits were also more prevalent in 'RQ001-02M2'. CONCLUSIONS: This study demonstrates for the first time at the cellular level that resistance to S. sclerotiorum in B. napus is a result of retardation of pathogen development, both on the plant surface and within host tissues. The resistance mechanisms identified in this study will be useful for engineering disease-resistant genotypes and for developing markers for screening for resistance against this pathogen.

Wheat stripe rust caused by Puccinia striiformis Westend. f.sp. tritici (Pst) is a global threat to wheat production. Genetic modification of defense-responsive factors in wheat rust interactions could help devise strategies to control stripe rust on wheat. This experiment studied the interaction between Pst pathotype 78S84 in PBW343 and FLW-3 by evaluating the quantitative temporal transcription profiles of defense-related genes at different time points. This is the first attempt to exhibit inter-connections among different proteins and depict a hypothetical model for the mechanism of R gene-mediated resistance. Transcript levels of LTP, AQP1, PR1, PR2, PR4, and PR10 were relatively higher under compatible interaction, while under incompatible interaction, transcript levels of COMT1, PRA2, WCAB, and PR9 were significantly high. This study projected the role of defense-responsive genes, inter-networking of proteins, and R gene-mediated resistance between wheat and stripe rust.

is a hemibiotrophic fungus that causes blackleg of canola ( ), one of the most devastating diseases of this crop. In the present study, transcriptome profiling of was performed in an effort to understand and define the pathogenicity genes that govern both the biotrophic and the necrotrophic phase of the fungus, as well as those that separate a compatible from an incompatible interaction. For this purpose, comparative RNA-seq analyses were performed on isolate D5 at four different time points following inoculation on susceptible cultivar Topas-DH16516 or resistant introgression line Topas- . Analysis of 1.6 billion Illumina reads readily identified differentially expressed genes that were over represented by candidate secretory effector proteins, CAZymes, and other pathogenicity genes. Comparisons between the compatible and incompatible interactions led to the identification of 28 effector proteins whose chronology and level of expression suggested a role in the establishment and maintenance of biotrophy with the plant. These included all known genes of isolate D5 along with eight newly characterized effectors. In addition, another 15 effector proteins were found to be exclusively expressed during the necrotrophic phase of the fungus, which supports the concept that has a separate and distinct arsenal contributing to each phase. As for CAZymes, they were often highly expressed at 3 dpi but with no difference in expression between the compatible and incompatible interactions, indicating that other factors were necessary to determine the outcome of the interaction. However, their significantly higher expression at 11 dpi in the compatible interaction confirmed that they contributed to the necrotrophic phase of the fungus. A notable exception was genes whose high expression was singularly observed on the susceptible host at 7 dpi. In the case of TFs, their higher expression at 7 and 11 dpi on susceptible Topas support an important role in regulating the genes involved in the different pathogenic phases of . In conclusion, comparison of the transcriptome of during compatible and incompatible interactions has led to the identification of key pathogenicity genes that regulate not only the fate of the interaction but also lifestyle transitions of the fungus.