The completion of the genome sequences of both rice and Magnaporthe oryzae has strengthened the position of rice blast disease as a model to study plant–pathogen interactions in monocotyledons. Genetic studies of blast resistance in rice were established in Japan as early as 1917. Despite such long-term study, examples of cultivars with durable resistance are rare, partly due to our limited knowledge of resistance mechanisms. A rising number of blast resistance genes and quantitative trait loci (QTL) have been genetically described, and some have been characterized during the last 20 years. Using the rice genome sequence, can we now go a step further toward a better understanding of the genetics of blast resistance by combining all these results? Is such knowledge appropriate and sufficient to improve breeding for durable resistance? A review of bibliographic references identified 85 blast resistance genes and approximately 350 QTL, which we mapped on the rice genome. These data provide a useful update on blast resistance genes as well as new insights to help formulate hypotheses about the molecular function of blast QTL, with special emphasis on QTL for partial resistance. All these data are available from the OrygenesDB database.

Background: Nitrogen often increases disease susceptibility, a phenomenon that can be observed under controlled conditions and called NIS, for Nitrogen-Induced Susceptibility. NIS has long been reported in the case of rice blast disease caused by the fungus Magnaporthe oryzae. We used an experimental system that does not strongly affect plant development to address the question of NIS polymorphism across rice diversity and further explored this phenomenon in wheat. We tested the two major types of resistance, namely quantitative/partial resistance and resistance driven by known resistance genes. Indeed there are conflicting reports on the effects of NIS on the first one and none on the last one. Finally, the genetics of NIS is not well documented and only few loci have been identified that may control this phenomenon. Results: Our data indicate that NIS is a general phenomenon affecting resistance to blast fungus in these two cereals. We show that the capacity of rice to display NIS is highly polymorphic and does not correlate with difference related to indica/japonica sub-groups. We also tested the robustness of three different major resistance genes under high nitrogen. Nitrogen partially breaks down resistance triggered by the Pi1 gene. Cytological examination indicates that penetration rate is not affected by high nitrogen whereas growth of the fungus is increased inside the plant. Using the CSSL mapping population between Nipponbare and Kasalath, we identified a Kasalath locus on chromosome 1, called NIS1, which dominantly increases susceptibility under high nitrogen. We discuss the possible relationships between Nitrogen Use Efficiency (NUE), disease resistance regulation and NIS. Conclusions: This work provides evidences that robust forms of partial resistance exist across diversity and can be easily identified with our protocol. This work also suggests that under certain environmental circumstances, complete resistance may breakdown, irrelevantly of the capacity of the fungus to mutate. These aspects should be considered while breeding for robust forms of resistance to blast disease.

Background: Partial resistance to plant pathogens is extensively used in breeding programs since it could contribute to resistance durability. Partial resistance often builds up during plant development and confers quantitative and usually broad-spectrum resistance. However, very little is known on the mechanisms underlying partial resistance. Partial resistance is often explained by poorly effective induction of plant defense systems. By exploring rice natural diversity, we asked whether expression of defense systems before infection could explain partial resistance towards the major fungal pathogen Magnaporthe oryzae. The constitutive expression of 21 defense-related genes belonging to the defense system was monitored in 23 randomly sampled rice cultivars for which partial resistance was measured. Results: We identified a strong correlation between the expression of defense-related genes before infection and partial resistance. Only a weak correlation was found between the induction of defense genes and partial resistance. Increasing constitutive expression of defense-related genes also correlated with the establishment of partial resistance during plant development. Some rice genetic sub-groups displayed a particular pattern of constitutive expression, suggesting a strong natural polymorphism for constitutive expression of defense. Constitutive levels of hormones like salicylic acid and ethylene cannot explain constitutive expression of defense. We could identify an area of the genome that contributes to explain both preformed defense and partial resistance. Conclusion: These results indicate that constitutive expression of defense-related genes is likely responsible for a large part of partial resistance in rice. The finding of this preformed defense system should help guide future breeding programs and open the possibility to identify the molecular mechanisms behind partial resistance.

Plants are often facing several stresses simultaneously. Understanding how they react and the way pathogens adapt to such combinational stresses is poorly documented. Here we developed an experimental system mimicking field intermittent drought on rice followed by inoculation by the pathogenic fungus Magnaporthe oryzae. This experimental system triggers an enhancement of susceptibility that could be correlated with the dampening of several aspects of plant immunity, namely the oxidative burst and the transcription of several pathogenesis-related genes. Quite strikingly, the analysis of fungal transcription by RNASeq analysis under drought reveals that the fungus is greatly modifying its virulence program: genes coding for small secreted proteins were massively repressed in droughted plants compared to unstressed ones whereas genes coding for enzymes involved in degradation of cell-wall were induced. We also show that drought can lead to the partial breakdown of several major resistance genes by affecting R plant gene and/or pathogen effector expression. We propose a model where a yet unknown plant signal can trigger a change in the virulence program of the pathogen to adapt to a plant host that was affected by drought prior to infection.

Understanding why nitrogen fertilization increase the impact of many plant diseases is of major importance. The interaction between Magnaporthe oryzae and rice was used as a model for analyzing the molecular mechanisms underlying Nitrogen-Induced Susceptibility (NIS). We show that our experimental system in which nitrogen supply strongly affects rice blast susceptibility only slightly affects plant growth. In order to get insights into the mechanisms of NIS, we conducted a dual RNA-seq experiment on rice infected tissues under two nitrogen fertilization regimes. On the one hand, we show that enhanced susceptibility was visible despite an over-induction of defense gene expression by infection under high nitrogen regime. On the other hand, the fungus expressed to high levels effectors and pathogenicity-related genes in plants under high nitrogen regime. We propose that in plants supplied with elevated nitrogen fertilization, the observed enhanced induction of plant defense is over-passed by an increase in the expression of the fungal pathogenicity program, thus leading to enhanced susceptibility. Moreover, some rice genes implicated in nitrogen recycling were highly induced during NIS. We further demonstrate that the OsGS1-2 glutamine synthetase gene enhances plant resistance to M. oryzae and abolishes NIS and pinpoint glutamine as a potential key nutrient during NIS.

• Our view of genes involved in rice disease resistance is far from complete. Here we used a gene-for-gene relationship corresponding to the interaction between atypical avirulence gene ACE1 from Magnaporthe grisea and rice resistance gene Pi33 to better characterize early rice defence responses induced during such interaction. • Rice genes differentially expressed during early stages of Pi33/ACE1 interaction were identified using DNA chip-based differential hybridization and QRT-PCR survey of the expression of known and putative regulators of disease resistance. • One hundred genes were identified as induced or repressed during rice defence response, 80% of which are novel, including resistance gene analogues. Pi33/ACE1 interaction also triggered the up-regulation of classical PR defence genes and a massive down-regulation of chlorophyll a/b binding genes. Most of these differentially expressed genes were induced or repressed earlier in Pi33/ACE1 interaction than in the gene–for–gene interaction involving Nipponbare resistant cultivar. • Besides demonstrating that an ACE1/Pi33 interaction induced classical and specific expression patterns, this work provides a list of new genes likely to be involved in rice disease resistance.