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 (22°C) compared with the normal growth temperature (28°C) 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 28°C but not at 22°C. Phenotypic analyses of the osaoc1 and osmyc2 mutants, OsCOI1 RNAi lines, and OsMYC2-OE plants further demonstrated that compromised M. oryzae-induced 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 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 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.
Keywords: CEBiP; MYB22; jasmonic acid; plant immunity; rice blast; temperature-modulated resistance.
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