Investigating the Induced Systemic Resistance Mechanism of 2,4-Diacetylphloroglucinol (DAPG) using DAPG Hydrolase-Transgenic Arabidopsis

The Plant Pathology Journal

Da-Ran Kim¹  Mi Sun Cheong²  Dae-Han Chae²  Yong Bok Lee²  Youn-Sig Kwak² 

[1] Department of Plant Medicine, Gyeongsang National University, Jinju 52828, Korea;Division of Applied Life Science (BK21Plus) and Institute of Agriculture & Life Science, Gyeongsang National University, Jinju 52828, Korea;

关键词: 2;    4-diacetylphloroglucinol (dapg);    antimicrobial;    induced systemic resistance (isr);    phlg;    pseudomonas;   

DOI  :  10.5423/PPJ.OA.02.2020.0031

来源: DOAJ

【 摘 要 】

Plant immune responses can be triggered by chemicals, microbes, pathogens, insects, or abiotic stresses. In particular, induced systemic resistance (ISR) refers to the activation of the immune system due to a plant’s interaction with beneficial microorganisms. The phenolic compound, 2,4-diacetylphloroglucinol (DAPG), which is produced by beneficial Pseudomonas spp., acts as an ISR elicitor, yet DAPG’s mechanism in ISR remains unclear. In this study, transgenic Arabidopsis thaliana plants overexpressing the DAPG hydrolase gene (phlG) were generated to investigate the functioning of DAPG in ISR. DAPG was applied onto 3-week-old A. thaliana Col-0 and these primed plants showed resistance to the pathogens Botrytis cinerea and Pseudomonas syringae pv. tomato DC3000. However, in the phlG transgenic A. thaliana, the ISR was not triggered against these pathogens. The DAPG-mediated ISR phenotype was impaired in transgenic A. thaliana plants overexpressing phlG, thus showing similar disease severity when compared to untreated control plants. Furthermore, the DAPG-treated A. thaliana Col-0 showed an increase in their gene expression levels of PDF1.2 and WRKY70 but this failed to occur in the phlG transgenic lines. Collectively, these experimental results indicate that jasmonic acid/ethylene signal-based defense system is effectively disabled in phlG transgenic A. thaliana lines.

【 授权许可】

Unknown