LAUSR

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, compared with rice normal growth temperature (28 °C), enhanced blast development at the warm temperature (22 °C) is rice plant-determined. Further comparative transcriptome analysis revealed that rice JA (jasmonic acid) biosynthesis and signaling genes could be effectively induced by Magnaporthe oryzae at 28 °C but not at 22 °C. Phenotypic analyses of the osaoc1 and osmyc2 mutants, OsCOI1 RNAi plants, and OsMYC2-OE plants demonstrated that compromised M. oryzae-induced JA biosynthesis and signaling led to enhanced blast susceptibility at the warm temperature. Consistent with these results, this study found that the application of MeJA was an effective strategy for improving blast resistance under the warm environment condition. Furthermore, decreased activation of JA signaling resulted in the down-regulated expressions of some basal resistance genes at 22 °C when compared with 28 °C. Among these affected genes, OsCEBiP (chitin elicitor-binding protein precursor) was found to be directly regulated by OsMYB22 and its interacting protein OsMYC2, a key component in JA signaling, and contributed to temperature-modulated resistance. Taken together, these results suggest that warm temperature compromises rice basal resistance to enhance Magnaporthe oryzae infection by reducing JA biosynthesis and signaling, providing potential new strategies for managing rice blast disease under warm environment conditions.