State Key Laboratory of Rice Biology, China National Rice Research Institute, Hangzhou 311400, China.
Temasek Life Sciences Laboratory, and Department of Biological Sciences, 1 Research Link, National University of Singapore, Singapore 117604, Singapore.
Mol Plant. 2022 Apr 4;15(4):723-739. doi: 10.1016/j.molp.2022.02.014. Epub 2022 Feb 22.
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.
全球温度的变化深刻地影响着植物病害的发生。众所周知，稻瘟病在相对温暖的天气中很容易流行。然而，其分子机制尚不清楚。在这项研究中，我们表明，与正常生长温度（28°C）相比，温暖温度（22°C）下增强的稻瘟病发展是由水稻植株决定的。比较转录组分析表明，在 28°C 下，茉莉酸（JA）生物合成和信号基因可以在水稻中被稻瘟病菌有效诱导，但在 22°C 下则不行。osaoc1 和 osmyc2 突变体、OsCOI1 RNAi 系和 OsMYC2-OE 植物的表型分析进一步表明，JA 生物合成和信号受损导致在温暖温度下增强了稻瘟病的易感性。与这些结果一致，我们发现，茉莉甲酯的外源应用是在温暖环境条件下提高稻瘟病抗性的有效策略。此外，与 28°C 相比，在 22°C 时 JA 信号的激活降低导致一些关键基础抗性基因的表达下调。在受影响的基因中，发现 OsCEBiP（几丁质诱导结合蛋白前体）直接受 OsMYB22 和其相互作用蛋白 OsMYC2 调控，而 OsMYC2 是 JA 信号的关键组成部分，这有助于温度调节的稻瘟病抗性。总之，这些结果表明，温暖的温度通过降低 JA 生物合成和信号来损害水稻的基础抗性，并增强稻瘟病菌的感染，为在温暖气候条件下管理稻瘟病提供了新的策略。
