Ochsenbein Christian, Przybyla Dominika, Danon Antoine, Landgraf Frank, Göbel Cornelia, Imboden André, Feussner Ivo, Apel Klaus
Institute of Plant Sciences, Plant Genetics, Swiss Federal Institute of Technology (ETH), CH-8092 Zurich, Switzerland.
Plant J. 2006 Aug;47(3):445-56. doi: 10.1111/j.1365-313X.2006.02793.x. Epub 2006 Jun 21.
Upon a dark/light shift the conditional flu mutant of Arabidopsis starts to generate singlet oxygen (1O2) that is restricted to the plastid compartment. Distinct sets of genes are activated that are different from those induced by hydrogen peroxide/superoxide. One of the genes that is rapidly upregulated is EDS1 (enhanced disease susceptibility). The EDS1 protein has been shown to be required for the resistance to biotrophic pathogens and the accumulation of salicylic acid (SA) that enhances the defenses of a plant by inducing the synthesis of pathogen-related (PR) proteins. Because of the similarity of its N-terminal portion to the catalytic site of lipases, EDS1 has also been implicated with the release of polyunsaturated fatty acids and the subsequent formation of various oxylipins. The release of singlet oxygen in the flu mutant triggers a drastic increase in the concentration of free SA and activates the expression of PR1 and PR5 genes. These changes depend on the activity of EDS1 and are suppressed in flu/eds1 double mutants. Soon after the beginning of singlet oxygen production, the synthesis of oxylipins such as jasmonic acid (JA) and 12-oxophytodienoic acid (OPDA) also start and plants stop growing and induce a cell-death response. The inactivation of EDS1 does not affect oxylipin synthesis, growth inhibition and the initiation of cell death, but it does allow plants to recover much faster from singlet oxygen-mediated growth inhibition and it also suppresses the spread of necrotic lesions in leaves. Hence, singlet oxygen activates a complex stress-response program with EDS1 playing a key role in initiating and modulating several steps of it. This program includes not only responses to oxidative stress, but also responses known to be activated during plant-pathogen interactions and wounding.
在黑暗/光照转换时，拟南芥的条件性流感突变体开始产生限于质体区室的单线态氧（1O₂）。不同组的基因被激活，这些基因与由过氧化氢/超氧阴离子诱导的基因不同。其中一个迅速上调的基因是EDS1（增强的疾病易感性）。EDS1蛋白已被证明是抵抗活体营养型病原体和水杨酸（SA）积累所必需的，SA通过诱导病程相关（PR）蛋白的合成来增强植物的防御能力。由于其N端部分与脂肪酶的催化位点相似，EDS1也与多不饱和脂肪酸的释放以及随后各种氧脂的形成有关。流感突变体中单线态氧的释放引发游离SA浓度的急剧增加，并激活PR1和PR5基因的表达。这些变化依赖于EDS1的活性，并在流感/eds1双突变体中受到抑制。在单线态氧产生开始后不久，茉莉酸（JA）和12-氧代植物二烯酸（OPDA）等氧脂的合成也开始，植物停止生长并诱导细胞死亡反应。EDS1的失活不影响氧脂合成、生长抑制和细胞死亡的启动，但它确实使植物能更快地从单线态氧介导的生长抑制中恢复，并且还抑制叶片中坏死病变的扩散。因此，单线态氧激活了一个复杂的应激反应程序，其中EDS1在启动和调节该程序的几个步骤中起关键作用。这个程序不仅包括对氧化应激的反应，还包括已知在植物-病原体相互作用和伤口处理过程中被激活的反应。
