Sustaining plant immunity in rising temperature
Sustaining plant immunity in rising temperature
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DOI：
10.1038/s41422-022-00710-1
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发表时间：
2022-08
期刊：
影响因子：
44.1
通讯作者：
J. Hua;Xinnian Dong
中科院分区：
文献类型：
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作者：
J. Hua;Xinnian Dong
在暴露于高温下时，一些植物免疫反应受到损害。在最近的一篇自然论文中，Kim等人表明，参与调节免疫信号水杨酸合成和信号传导的转录因子的异位表达可以在高温下维持免疫能力，这表明农业中对抗全球变暖的可能工程策略。温度是对植物及其与病原体相互作用有很大影响的主要环境因素。温度对植物免疫力的影响是复杂的，最普遍的相互作用是温度升高对植物免疫力的抑制。1这一现象首先是在温度从22 ℃升高到30 ℃时对烟草花叶病毒（TMV）的抗性完全丧失时观察到的。[2]后来发现这种抗性是由N基因赋予的，该基因是利用一种基于抗性的温度敏感性而开发的巧妙选择方案克隆的。3 N基因是植物细胞内核苷酸结合位点和富含亮氨酸重复结构域（NLR）免疫受体基因的创始成员。从那时起，几个额外的NLR已被证明对升高的温度敏感。4除了抑制对TMV的局部抗性外，将温度升高到26 ℃还阻断了在未处理组织中建立系统获得抗性（SAR），5这是一种广谱抗性机制，后来发现需要产生免疫信号水杨酸（SA）。与这些早期的观察结果一致，发现参与SA生物合成的基因如CBP 60 g和ICS 1，以及参与SA信号传导的基因如PAD 4和EDS 1的表达在30 ℃下被显著抑制。随着全球气候变化，植物免疫系统对热的敏感性对全球粮食供应和生态系统构成了巨大威胁。如何在温暖的气候中维持植物免疫力是一个迫切需要克服的挑战。在《自然》杂志最近的一份报告中，7 Kim和Sheng Yang He小组的同事开发了一种解决方案，该解决方案涉及编码大量植物免疫基因的主转录因子的CBP 60g基因的组成型表达，以恢复SA生产和高温下的抗病性。正常情况下，由于鸟苷酸结合蛋白样3（GBPL 3）将介体复合物（MED）和RNA聚合酶II（POL II）机制的转录共激活因子募集至CBP 60 g启动子而形成的GBPL防御激活缩合物（GDAC）数量减少，温度升高会抑制CBP 60 g的表达。这项研究揭示了GBPL 3作为植物免疫中的一种新的温度传感器，基于其物理性质，即冷凝物形成，将温度与防御基因转录联系起来（图1）。
Upon exposure to high temperature, some plant immune responses are compromised. In a recent Nature paper, Kim et al. show that ectopic expression of transcription factors involved in regulating the immune signal salicylic acid synthesis and signaling could sustain immune competency at high temperature, suggesting a possible engineering strategy for fighting global warming in agriculture.Temperature is a major environmental factor that has a large impact on plants and their interactions with pathogens. The temperature effect on plant immunity is complex, with the most prevalent interaction being the suppression of plant immunity by elevated temperature. 1 This phenomenon was first observed as the complete loss of resistance to tobacco mosaic virus (TMV) when temperature was raised from 22 C to 30 C. 2 This resistance was later found to be conferred by the N gene, which was cloned using a clever selection scheme developed based on the temperature sensitivity of the resistance. 3 The N gene is a founding member of intracellular nucleotide-binding site and leucine-rich repeat domain (NLR) immune receptor genes in plants. Since then, several additional NLRs have been shown to be sensitive to elevated temperature. 4 In addition to inhibiting local resistance to TMV, elevating temperature to 26 C also blocks the establishment of systemic acquired resistance (SAR) in naïve tissues, 5 a broadspectrum resistance mechanism which was later found to require the production of the immune signal salicylic acid (SA). Consistent with these earlier observations, expression of genes involved in SA biosynthesis, such as CBP60g and ICS1, and SA signaling, such as PAD4 and EDS1, was found to be significantly inhibited at 30 C. 6 With global climate change, susceptibility of the plant immune system to heat poses a great threat to global food supply and the ecosystem. How to sustain plant immunity in a warmer climate is an urgent challenge that needs to be overcome. In a recent report in Nature, 7 Kim and colleagues in Sheng Yang He’s group have developed a solution which involves constitutive expression of the CBP60g gene encoding a master transcription factor of a large number of plant immunity genes to restore SA production and disease resistance at elevated temperature. Normally, expression of CBP60g is inhibited by increased temperature due to the reduced number of GBPL defense-activated condensates (GDAC) formed by GUANYLATE BINDING PROTEIN-LIKE 3 (GBPL3) to recruit transcriptional coactivators of the Mediator complex (MED) and the RNA polymerase II (POL II) machinery to the CBP60g promoter. This study reveals GBPL3 as a new temperature sensor in plant immunity based on its physical property, ie, condensate formation, connecting temperature to defense gene transcription (Fig. 1).