Oligogalacturonides induce resistance in Arabidopsis thaliana by triggering salicylic acid and jasmonic acid pathways against Pst DC3000
Oligogalacturonides induce resistance in Arabidopsis thaliana by triggering salicylic acid and jasmonic acid pathways against Pst DC3000
复制标题
低聚半乳糖醛酸通过触发水杨酸和茉莉酸途径对抗 Pst DC3000，诱导拟南芥产生抗性
DOI：
10.1016/j.ijbiomac.2020.09.026
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发表时间：
2020-12-01
影响因子：
8.2
通讯作者：
Yin, Heng
中科院分区：
文献类型：
--
作者：
Howlader, Prianka;Bose, Santosh Kumar;Yin, Heng
寡聚半乳糖醛酸（OGA）是一种生物活性碳水化合物，来源于高半乳糖醛酸聚糖，细胞壁果胶的主要成分。研究了OGA诱导拟南芥-假单胞菌pv.番茄DC 3000（Pst DC 3000）互作。25 mg/L OGAs处理对黄瓜枯萎病的有效抗性主要表现在病情指数降低、细菌增殖减少、水杨酸（SA）途径相关基因（PR 1、PR 2、PR 5）和茉莉酸（JA）途径相关基因（PDF 1. 2、VSP 2）的转录水平升高、SA、JA含量增加、活性氧（ROS）和一氧化氮（NO）产生增加。在SA（NahG，NH 2）和JA（jar 1）缺陷突变体中，病害严重程度表明SA和JA途径对于拟南芥对Pst DC 3000的响应是必需的。JA缺失突变体和SA缺失突变体对Pst DC 3000的抗性较低，表明SA和JA在OGA诱导的抗性中起冗余作用。因此，这些证据进一步揭示了OGA抗性的信号转导途径，有利于其在农业上的应用，以保护植物免受疾病的侵害。(C)2020爱思唯尔B. V.保留所有权利。
Oligogalacturonides (OGAs) are a biologically active carbohydrate derived from homogalacturonan, a major element of cell wall pectin. OGAs induced resistance and mechanism were assessed in Arabidopsis thaliana-Pseudomonas syringae pv. tomato DC3000 (Pst DC3000) interaction. The effective resistance was mainly observed at 25 mg/L OGAs with reduced disease index, bacterial multiplication, higher transcript level of salicylic acid (SA) pathway related genes (PR1, PR2, PR5) and jasmonic acid (JA) pathway related genes (PDF1.2, VSP2) as well as SA, JA content and production of reactive oxygen species (ROS), nitric oxide (NO). In SA (NahG, sid2) and JA (jar1) deficient mutants, disease severity indicated that both SA and JA pathways are necessary for Arabidopsis response to Pst DC3000. OGAs triggered less resistance to Pst DC3000 in JA-deficient mutant, and SA-deficient mutants signifying that SA and JA play redundant roles in OGAs induced resistance. Therefore, these evidences further reveal the signaling pathways of OGAs resistance, which is conducive to its application in agriculture to protect plants from diseases. (C) 2020 Elsevier B.V. All rights reserved.