The Arabidopsis flavin-dependent monooxygenase FMO1 is an essential component of biologically induced systemic acquired resistance
The Arabidopsis flavin-dependent monooxygenase FMO1 is an essential component of biologically induced systemic acquired resistance
复制标题
DOI：
10.1104/pp.106.081257
复制
发表时间：
2006-08-01
期刊：
影响因子：
7.4
通讯作者：
Zeier, Juergen
中科院分区：
文献类型：
--
作者：
Mishina, Tatiana E.;Zeier, Juergen
在坏死性病原体的局部攻击后，植物在整个植物水平上逐渐发展出对随后感染的抗性，这种现象称为系统获得性抗性（SAR）。为了确定参与SAR建立的基因，我们采用了一种策略，将来自微阵列数据的基因表达信息与所选拟南芥（Arabidopsis thaliana）T-DNA插入系的病理特征相结合。在接种细菌病原体假单胞菌斑点致病变种（Psm）的无毒或有毒菌株的拟南芥叶片中上调的基因显示与黄素依赖性单加氧酶（FMO）同源，并被命名为FMO 1。一个拟南芥敲除系的FMO 1被证明是完全受损的建立SAR触发的毒性（Psm avrRpm 1）或毒性（Psm）细菌。fmo 1突变体中SAR的丧失伴随着不能启动水杨酸（SA）的系统积累和多种防御相关基因的系统表达。与此相反，在病原体攻击的网站，包括防御信号SA和茉莉酸，camalexin积累，和各种防御基因的表达水平的增加的反应，诱导以类似的方式在fmo 1突变体和野生型植物。一致的是，fmo 1突变并没有显着影响本地抗病性对毒力或无毒力的细菌在幼稚植物。在病原体接种位点诱导FMO 1表达不依赖于SA信号，但在拟南芥eds 1和pad 4防御突变体中减弱。重要的是，FMO 1的表达也是在局部的P. eriningae感染后全身诱导的。这种系统性上调在SAR缺陷型SA途径突变体NDR 2和npr 1以及防御突变体ndr 1中缺失，表明系统性FMO 1表达与SAR建立之间存在密切相关性。我们的研究结果表明，系统组织中的FMO 1基因产物的存在是至关重要的SAR的发展，可能是通过合成的代谢产物所需的信号转导或放大在早期阶段的SAR建立系统叶。
Upon localized attack by necrotizing pathogens, plants gradually develop increased resistance against subsequent infections at the whole-plant level, a phenomenon known as systemic acquired resistance (SAR). To identify genes involved in the establishment of SAR, we pursued a strategy that combined gene expression information from microarray data with pathological characterization of selectedArabidopsis ( Arabidopsis thaliana) T-DNA insertion lines. A gene that is up-regulated in Arabidopsis leaves inoculated with avirulent or virulent strains of the bacterial pathogen Pseudomonas syringae pv maculicola (Psm) showed homology to flavin-dependent monooxygenases (FMO) and was designated as FMO1. An Arabidopsis knockout line of FMO1 proved to be fully impaired in the establishment of SAR triggered by a virulent (Psm avrRpm1) or virulent ( Psm) bacteria. Loss of SAR in the fmo1 mutants was accompanied by the inability to initiate systemic accumulation of salicylic acid ( SA) and systemic expression of diverse defense-related genes. In contrast, responses at the site of pathogen attack, including increases in the levels of the defense signals SA and jasmonic acid, camalexin accumulation, and expression of various defense genes, were induced in a similar manner in both fmo1 mutant and wild-type plants. Consistently, the fmo1 mutation did not significantly affect local disease resistance toward virulent or avirulent bacteria in naive plants. Induction of FMO1 expression at the site of pathogen inoculation is independent of SA signaling, but attenuated in the Arabidopsis eds1 and pad4 defensemutants. Importantly, FMO1 expression is also systemically induced upon localized P. syringae infection. This systemic up-regulation is missing in the SAR-defective SA pathway mutants sid2 and npr1, as well as in the defense mutant ndr1, indicating a close correlation between systemic FMO1 expression and SAR establishment. Our findings suggest that the presence of the FMO1 gene product in systemic tissue is critical for the development of SAR, possibly by synthesis of a metabolite required for the transduction or amplification of a signal during the early phases of SAR establishment in systemic leaves.