2,4-Diacetylphloroglucinol (DAPG) Enhances Induced Systemic Resistance Against Necrotrophic Pathogens Through the COI1-Mediated JA Signaling Pathway in Arabidopsis
- Authors
- Kim, Sun Ho; Kwon, Young Sang; Nguyen, Cam Chau; Pham, Minh Le Anh; Ma, Yuqiao; Lee, Kyunghee; Bae, Dong-Won; Chin, Hang Gyeong; Chung, Woo Sik
- Issue Date
- Aug-2025
- Publisher
- Springer Verlag
- Keywords
- Arabidopsis; 2,4-Diacetylphloroglucino; Jasmonic acid; Necrotrophic pathogen; Resistance
- Citation
- Journal of Plant Growth Regulation, v.44, no.8, pp 4881 - 4890
- Pages
- 10
- Indexed
- SCIE
SCOPUS
- Journal Title
- Journal of Plant Growth Regulation
- Volume
- 44
- Number
- 8
- Start Page
- 4881
- End Page
- 4890
- URI
- https://scholarworks.gnu.ac.kr/handle/sw.gnu/78204
- DOI
- 10.1007/s00344-025-11729-0
- ISSN
- 0721-7595
1435-8107
- Abstract
- 2,4-Diacetylphloroglucinol (DAPG) is a polyketide antibiotic and secondary metabolite produced by various strains of fluorescent Pseudomonas spp. It plays a crucial role in biological control by triggering induced systemic resistance (ISR) against pathogens in plants. However, the molecular mechanisms underlying DAPG's action remain unclear. Building on our previous research, which showed that DAPG-treated Arabidopsis leaves exhibit increased expression of jasmonic acid (JA) biosynthesis and responsive proteins, we investigated the effects of DAPG on resistance against the necrotrophic pathogens Botrytis cinerea in Arabidopsis. Our results demonstrated that DAPG treatment significantly reduced necrosis caused by B. cinerea infection. Additionally, JA levels were notably elevated following DAPG treatment due to the transcriptional up-regulation of JA biosynthesis genes, resulting in enhanced JA responses. Importantly, DAPG-induced plant resistance against B. cinerea was compromised in the JA-insensitive mutant (coi1-1). These findings suggest that DAPG enhances resistance to necrotrophic pathogen by activating JA signaling, highlighting its potential as a crucial factor in boosting plant immunity.
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