Abstract
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), JAdependent 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.