Systemic acquired resistance in Cavendish banana induced by infection with an incompatible strain of Fusarium oxysporum f. sp. cubense |
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Authors: | Yuanli Wu Ganjun Yi Xinxiang Peng Bingzhi Huang Ee Liu Jianjun Zhang |
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Affiliation: | 1. Fruit Tree Research Institute, Guangdong Academy of Agricultural Sciences, Guangzhou 510640, China;2. Key Laboratory of South Subtropical Fruit Biology and Genetic Resource Utilization, Ministry of Agriculture, China;3. College of Life Sciences, South China Agricultural University, Guangzhou 510642, China |
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Abstract: | Fusarium wilt of banana is caused by the soil-borne fungus Fusarium oxysporum f. sp. cubense (Foc). The fact that there are no economically viable biological, chemical, or cultural measures of controlling the disease in an infected field leads to search for alternative strategies involving activation of the plant's innate defense system. The mechanisms underlying systemic acquired resistance (SAR) are much less understood in monocots than in dicots. Since systemic protection of plants by attenuated or avirulent pathogens is a typical SAR response, the establishment of a biologically induced SAR model in banana is helpful to investigate the mechanism of SAR to Fusarium wilt. This paper described one such model using incompatible Foc race 1 to induce resistance against Foc tropical race 4 in an in vitro pathosystem. Consistent with the observation that the SAR provided the highest level of protection when the time interval between primary infection and challenge inoculation was 10 d, the activities of defense-related enzymes such as phenylalanine ammonia lyase (PAL, EC 4.3.1.5), peroxidase (POD, EC 1.11.1.7), polyphenol oxidase (PPO, EC 1.14.18.1), and superoxide dismutase (SOD, EC 1.15.1.1) in systemic tissues also reached the maximum level and were 2.00–2.43 times higher than that of the corresponding controls on the tenth day. The total salicylic acid (SA) content in roots of banana plantlets increased from about 1 to more than 5 μg g−1 FW after the second leaf being inoculated with Foc race 1. The systemic up-regulation of MaNPR1A and MaNPR1B was followed by the second up-regulation of PR-1 and PR-3. Although SA and jasmonic acid (JA)/ethylene (ET) signaling are mostly antagonistic, systemic expression of PR genes regulated by different signaling pathways were simultaneously up-regulated after primary infection, indicating that both pathways are involved in the activation of the SAR. |
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Keywords: | BTH, benzothiadiazole ET, ethylene ETI, effector-triggered immunity Foc, Fusarium oxysporum f. sp. cubense FW, fresh weight HR, hypersensitive response IAA, indoleacetic acid INA, 2,6-dichloroisonicotinic acid ISR, induced systemic resistance JA, jasmonic acid MIS, medium for interaction system MS, Murashige and Skoog medium NBT, nitroblue tetrazolium nkat, nanokatals NPR1, nonexpressor of pathogenesis-related genes 1 PAL, phenylalanine ammonia lyase PAMPs, pathogen associated molecular patterns PGPR, plant growth-promoting rhizobacteria pkat, picokatals POD, peroxidase PPO, polyphenol oxidase PR gene, pathogenesis-related gene PRRs, pattern-recognition receptors PTI, pattern-triggered immunity SA, salicylic acid SAR, systemic acquired resistance SOD, superoxide dismutase |
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