Department of Molecular Phytopathology and Biotechnology, Institute of Phytopathology, Christian-Albrechts Universität zu Kiel, 24118, Kiel, Germany.
Department of Molecular Phytopathology and Biotechnology, Institute of Phytopathology, Christian-Albrechts Universität zu Kiel, 24118, Kiel, Germany.
Plant Physiol Biochem. 2019 Jan;134:53-63. doi: 10.1016/j.plaphy.2018.06.026. Epub 2018 Jun 22.
Plants respond to abiotic UV-B stress with enhanced expression of genes for flavonoid production, especially the key-enzyme chalcone synthase (CHS). Some flavonoids are antioxidative, antimicrobial and/or UV-B protective secondary metabolites. However, when plants are challenged with concomitant biotic stress (simulated e.g. by the bacterial peptide flg22, which induces MAMP triggered immunity, MTI), the production of flavonoids is strongly suppressed in both Arabidopsis thaliana cell cultures and plants. On the other hand, flg22 induces the production of defense related compounds, such as the phytoalexin scopoletin, as well as lignin, a structural barrier thought to restrict pathogen spread within the host tissue. Since all these metabolites require the precursor phenylalanine for their production, suppression of the flavonoid production appears to allow the plant to focus its secondary metabolism on the production of pathogen defense related compounds during MTI. Interestingly, several flavonoids have been reported to display anti-microbial activities. For example, the plant flavonoid phloretin targets the Pseudomonas syringae virulence factors flagella and type 3 secretion system. That is, suppression of flavonoid synthesis during MTI might have also negative side-effects on the pathogen defense. To clarify this issue, we deployed an Arabidopsis flavonoid mutant and obtained genetic evidence that flavonoids indeed contribute to ward off the virulent bacterial pathogen Pseudomonas syringae pv. tomato (Pst) DC3000. Finally, we show that UV-B attenuates expression of the flg22 receptor FLS2, indicating that there is negative and reciprocal interaction between this abiotic stress and the plant-pathogen defense responses.
植物通过增强类黄酮生物合成相关基因的表达来应对非生物 UV-B 胁迫，尤其是关键酶查尔酮合酶（CHS）。一些类黄酮是抗氧化、抗菌和/或 UV-B 保护的次生代谢物。然而，当植物同时受到生物胁迫（例如通过模拟细菌肽 flg22 来诱导模式触发免疫，MTI）的挑战时，类黄酮的合成在拟南芥细胞培养物和植物中都会受到强烈抑制。另一方面，flg22 诱导防御相关化合物的产生，如植保素伞形酮以及木质素，木质素被认为是一种结构屏障，可限制病原体在宿主组织内的传播。由于所有这些代谢物的产生都需要苯丙氨酸作为前体，因此类黄酮的合成受到抑制似乎使植物能够在 MTI 期间将其次生代谢集中于产生与病原体防御相关的化合物。有趣的是，已经有报道称几种类黄酮具有抗微生物活性。例如，植物类黄酮 phloretin 靶向 Pseudomonas syringae 毒力因子鞭毛和 III 型分泌系统。也就是说，在 MTI 期间抑制类黄酮合成可能对病原体防御也有负面影响。为了澄清这个问题，我们利用拟南芥类黄酮突变体获得了遗传证据，表明类黄酮确实有助于抵御强毒力的细菌病原体 Pseudomonas syringae pv. tomato (Pst) DC3000。最后，我们表明 UV-B 会减弱 flg22 受体 FLS2 的表达，表明这种非生物胁迫与植物-病原体防御反应之间存在负向和相互的相互作用。
