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Alleviating protein-condensation-associated damage at the endoplasmic reticulum enhances plant disease tolerance
Cell Host & Microbe ( IF 20.6 ) Pub Date : 2024-08-06 , DOI: 10.1016/j.chom.2024.07.013
Zhijuan Tang 1 , Shaosong Shi 1 , Ruixia Niu 1 , Yulu Zhou 1 , Zhao Wang 1 , Rongrong Fu 1 , Rui Mou 1 , Suming Chen 1 , Pingtao Ding 2 , Guoyong Xu 3
Affiliation  

Disease tolerance is an essential defense strategy against pathogens, alleviating tissue damage regardless of pathogen multiplication. However, its genetic and molecular basis remains largely unknown. Here, we discovered that protein condensation at the endoplasmic reticulum (ER) regulates disease tolerance in Arabidopsis against Pseudomonas syringae. During infection, Hematopoietic protein-1 (HEM1) and Bax-inhibitor 1 (BI-1) coalesce into ER-associated condensates facilitated by their phase-separation behaviors. While BI-1 aids in clearing these condensates via autophagy, it also sequesters lipid-metabolic enzymes within condensates, likely disturbing lipid homeostasis. Consequently, mutations in hem1, which hinder condensate formation, or in bi-1, which prevent enzyme entrapment, enhance tissue-damage resilience, and preserve overall plant health during infection. These findings suggest that the ER is a crucial hub for maintaining cellular homeostasis and establishing disease tolerance. They also highlight the potential of engineering disease tolerance as a defense strategy to complement established resistance mechanisms in combating plant diseases.

中文翻译:


减轻内质网的蛋白质凝聚相关损伤可增强植物对病害的耐受性



疾病耐受性是抵御病原体的重要防御策略,无论病原体如何繁殖,都能减轻组织损伤。然而,它的遗传和分子基础在很大程度上仍然未知。在这里,我们发现内质网 (ER) 的蛋白质浓缩调节拟南芥对丁香假单胞菌的疾病耐受性。在感染过程中,造血蛋白 1 (HEM1) 和 Bax 抑制剂 1 (BI-1) 通过它们的相分离行为聚结成 ER 相关凝聚物。虽然 BI-1 有助于通过自噬清除这些凝聚物,但它也会将脂质代谢酶隔离在凝聚物中,这可能会干扰脂质稳态。因此,hem1 中的突变会阻碍凝聚物的形成,而 bi-1 中的突变会阻止酶的包埋,增强组织损伤的恢复力,并在感染期间保持植物的整体健康。这些发现表明 ER 是维持细胞稳态和建立疾病耐受性的关键枢纽。他们还强调了工程抗病性作为一种防御策略的潜力,以补充对抗植物病害的既定抗性机制。
更新日期:2024-08-06
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