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Increasing the resilience of plant immunity to a warming climate
Nature ( IF 50.5 ) Pub Date : 2022-06-29 , DOI: 10.1038/s41586-022-04902-y
Jong Hum Kim 1, 2, 3 , Christian Danve M Castroverde 3, 4, 5 , Shuai Huang 6, 7, 8 , Chao Li 9 , Richard Hilleary 1, 2, 3 , Adam Seroka 1, 2, 4, 10 , Reza Sohrabi 1, 2, 3, 4 , Diana Medina-Yerena 3 , Bethany Huot 1, 4 , Jie Wang 10 , Kinya Nomura 1, 2, 3 , Sharon K Marr 11 , Mary C Wildermuth 11 , Tao Chen 9 , John D MacMicking 6, 7, 8 , Sheng Yang He 1, 2, 3, 4, 10
Affiliation  

Extreme weather conditions associated with climate change affect many aspects of plant and animal life, including the response to infectious diseases. Production of salicylic acid (SA), a central plant defence hormone1,2,3, is particularly vulnerable to suppression by short periods of hot weather above the normal plant growth temperature range via an unknown mechanism4,5,6,7. Here we show that suppression of SA production in Arabidopsis thaliana at 28 °C is independent of PHYTOCHROME B8,9 (phyB) and EARLY FLOWERING 310 (ELF3), which regulate thermo-responsive plant growth and development. Instead, we found that formation of GUANYLATE BINDING PROTEIN-LIKE 3 (GBPL3) defence-activated biomolecular condensates11 (GDACs) was reduced at the higher growth temperature. The altered GDAC formation in vivo is linked to impaired recruitment of GBPL3 and SA-associated Mediator subunits to the promoters of CBP60g and SARD1, which encode master immune transcription factors. Unlike many other SA signalling components, including the SA receptor and biosynthetic genes, optimized CBP60g expression was sufficient to broadly restore SA production, basal immunity and effector-triggered immunity at the elevated growth temperature without significant growth trade-offs. CBP60g family transcription factors are widely conserved in plants12. These results have implications for safeguarding the plant immune system as well as understanding the concept of the plant–pathogen–environment disease triangle and the emergence of new disease epidemics in a warming climate.



中文翻译:

提高植物对气候变暖的免疫力

与气候变化相关的极端天气条件影响动植物生命的许多方面,包括对传染病的反应。水杨酸 (SA) 是一种重要的植物防御激素1,2,3,它的产生特别容易受到高于正常植物生长温度范围的短期炎热天气的抑制,其机制未知4,5,6,7。在这里,我们表明,在 28 °C 下拟南芥SA 产生的抑制与 PHYTOCHROME B 8,9 (phyB) 和 EARLY FLOWERING 3 10 (ELF3)无关,它们调节热响应性植物的生长和发育。相反,我们发现鸟苷酸结合蛋白样 3 (GBPL3) 防御激活生物分子缩合物11 (GDAC) 的形成在较高的生长温度下减少。体内 GDAC 形成的改变与 GBPL3 和 SA 相关介导亚基向编码主免疫转录因子的CBP60gSARD1启动子的募集受损有关。与许多其他 SA 信号成分(包括 SA 受体和生物合成基因)不同,优化的CBP60g表达足以在升高的生长温度下广泛恢复 SA 的产生、基础免疫和效应子触发的免疫,而无需显着的生长权衡。CBP60g 家族转录因子在植物中广泛保守12。这些结果对于保护植物免疫系统以及理解植物-病原体-环境疾病三角的概念以及气候变暖中新疾病流行的出现具有重要意义。

更新日期:2022-06-29
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