Warm temperature compromises JA-regulated basal resistance to enhance Magnaporthe oryzae infection in rice
Warm temperature compromises JA-regulated basal resistance to enhance Magnaporthe oryzae infection in rice
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DOI：
10.1016/j.molp.2022.02.014
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发表时间：
2022-04-06
期刊：
影响因子：
27.5
通讯作者：
Kou, Yanjun
中科院分区：
文献类型：
--
作者：
Qiu, Jiehua;Xie, Junhui;Kou, Yanjun
全球气温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很容易流行。然而，其分子机制仍不清楚。在这项研究中，我们表明，在温暖的温度（22摄氏度）与正常生长温度（28摄氏度）相比，稻瘟病的发展是由水稻植物决定的。比较转录组分析表明，稻瘟病菌在28 ℃下能有效诱导水稻茉莉酸（JA）生物合成和信号转导基因，而在22 ℃下则不能。对osaoc 1和osmyc 2突变体、OsCOI 1 RNAi株系和OsMYC 2-OE植株的表型分析进一步证明，受损的M.水稻诱导的JA生物合成和信号传导导致高温下稻瘟病易感性增强。与这些结果一致，我们发现，外源施用茉莉酸甲酯作为一种有效的策略，提高稻瘟病抗性在温暖的环境条件下。此外，与28 ℃相比，22 ℃时JA信号的激活减少导致一些关键的基础抗性基因的表达下调。在这些受影响的基因中，发现OsCEBiP（几丁质激发子结合蛋白前体）直接受OsMYB 22及其相互作用蛋白OsMYC 2（JA信号传导的关键组分）的调控，这有助于温度调节的稻瘟病抗性。这些结果表明，温暖的温度损害了水稻的基础抗性，提高了M。通过减少JA的生物合成和信号传导抑制稻瘟病的发生，为在温暖气候条件下控制稻瘟病提供了潜在的新策略。
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 degrees C) compared with the normal growth temperature (28 degrees 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 degrees C but not at 22 degrees 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 degrees C when compared with 28 degrees 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.