Salt Enhances Disease Resistance and Suppresses Cell Death in Ceramide Kinase Mutants
Salt Enhances Disease Resistance and Suppresses Cell Death in Ceramide Kinase Mutants
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盐增强神经酰胺激酶突变体的抗病能力并抑制细胞死亡
DOI：
10.1104/pp.19.00613
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发表时间：
2019-09-01
期刊：
影响因子：
7.4
通讯作者：
Yao, Nan
中科院分区：
文献类型：
--
作者：
Yang, Yu-Bing;Yin, Jian;Yao, Nan
鞘磷脂是细胞膜的结构成分，也是各种植物发育过程和防御反应的信号，包括细胞程序性死亡。最近的研究揭示了非生物或生物应激与细胞程序性死亡之间的相互作用。在先前的研究中，我们鉴定了一个拟南芥细胞死亡突变体，加速细胞死亡5(Acd5)，它积累神经酰胺并在发育后期表现出自发的细胞死亡。在这项工作中，我们报告了盐(氯化钠)处理抑制了acd5突变体中的细胞死亡，并防止了神经鞘脂脂的积累。外源应用脱落酸(ABA)和水杨酸(SA)类似物苯并噻二唑表明，NaCI的作用部分依赖于内源SA和ABA之间的拮抗作用。然而，使用缺乏ABA途径的突变体表明，完整的ABA途径可能不是这一效应所必需的。此外，盐预处理增强了对生物胁迫的抗性反应，这种增强的抗性不涉及病原菌相关的分子模式触发的免疫反应。综上所述，我们的发现表明，盐通过依赖SA和ABA拮抗相互作用的机制部分抑制了acd5突变体中鞘脂的积累和细胞死亡，并增强了不依赖于模式触发的免疫反应的抗病能力。
Sphingolipids act as structural components of cellular membranes and as signals in a variety of plant developmental processes and defense responses, including programmed cell death. Recent studies have uncovered an interplay between abiotic or biotic stress and programmed cell death. In a previous study, we characterized an Arabidopsis (Arabidopsis thaliana) cell-death mutant, accelerated cell death5 (acd5), which accumulates ceramides and exhibits spontaneous cell death late in development. In this work, we report that salt (NaCl) treatment inhibits cell death in the acd5 mutant and prevents the accumulation of sphingolipids. Exogenous application of abscisic acid (ABA) and the salicylic acid (SA) analog benzothiadiazole demonstrated that the effect of NaC1 was partly dependent on the antagonistic interaction between endogenous SA and ABA. However, the use of mutants deficient in the ABA pathway suggested that the intact ABA pathway may not be required for this effect. Furthermore, pretreatment with salt enhanced the resistance response to biotic stress, and this enhanced resistance did not involve the pathogen-associated molecular pattern-triggered immune response. Taken together, our findings indicate that salt inhibits sphingolipid accumulation and cell death in acd5 mutants partly via a mechanism that depends on SA and ABA antagonistic interaction, and enhances disease resistance independent of pattern-triggered immune responses.