Warm temperature compromises JA-regulated basal resistance to enhance Magnaporthe oryzae infection in rice

Changes in global temperatures profoundly affect the occurrence of plant diseases.It is well known that rice blast can easily become epidemic in relatively warm weather.However,the molecular mechanism remains unclear.In this study,we show that enhanced blast development at a warm temperature(22C)compared with the normal growth temperature(28C)is rice plant-determined.Comparative transcriptome analysis revealed that jasmonic acid(JA)biosynthesis and signaling genes in rice could be effectively induced by Magnaporthe oryzae at 28C but not at 22C.Phenotypic analyses of the osaoc1 and osmyc2 mutants,OsCOI1 RNAi lines,and OsMYC2-OE plants further demonstrated that compromised M.oryzaeinduced JA biosynthesis and signaling lead to enhanced blast susceptibility at the warm temperature.Consistent with these results,we found that exogenous application of methyl jasmonate served as an effective strategy for improving blast resistance under the warm environmental conditions.Furthermore,decreased activation of JA signaling resulted in the downregulated expression of some key basal resistance genes at 22C when compared with 28C.Among these affected genes,OsCEBiP(chitin elicitorbinding protein precursor)was found to be directly regulated by OsMYB22 and its interacting protein OsMYC2,a key component of JA signaling,and this contributed to temperature-modulated blast resistance.Taken together,these results suggest that warm temperature compromises basal resistance in rice and enhances M.oryzae infection by reducing JA biosynthesis and signaling,providing potential new strategies for managing rice blast disease under warm climate conditions.

The E3 ubiquitin ligase OsRGLG5 targeted by the Magnaporthe oryzae effector AvrPi9 confers basal resistance against rice blast

Rice blast,caused by Magnaporthe oryzae,is one of the most devastating diseases of rice.During infection,M.oryzae secretes effectors to facilitate blast development.Among these effectors,the avirulence factor AvrPi9 is recognized by Pi9,a broad-spectrum blast resistance protein that triggers Pi9-mediated resistance in rice.However,little is known about the interaction between AvrPi9 and Pi9 and how AvrPi9 exerts virulence to promote infection.In this study,we found that ectopic expression of AvrPi9 in the Pi9-lacking cultivar TP309 suppressed basal resistance against M.oryzae.Furthermore,we identified an AvrPi9-interacting protein in rice,which we named OsRGLG5,encoding a functional RING-type E3 ubiquitin ligase.During infection,AvrPi9 was ubiquitinated and degraded by OsRGLG5.Meanwhile,AvrPi9 affected the stability of OsRGLG5.Infection assays revealed that OsRGLG5 is a positive regulator of basal resistance against M.oryzae,but it is not essential for Pi9-mediated blast resistance in rice.In conclusion,our results revealed that OsRGLG5 is targeted by the M.oryzae effector AvrPi9 and positively regulates basal resistance against rice blast.