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首页> 外文期刊>Journal of Plant Physiology >Systemic acquired resistance in Cavendish banana induced by infection with an incompatible strain of Fusarium oxysporum f. sp. cubense.
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Systemic acquired resistance in Cavendish banana induced by infection with an incompatible strain of Fusarium oxysporum f. sp. cubense.

机译:卡文迪许香蕉的系统性获得性抗性是由不兼容的尖孢镰刀菌f菌株感染引起的。 sp。立方。

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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 micro g 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.
机译:香蕉枯萎病是由土传真菌尖孢镰刀菌f引起的。 sp。立方(Foc)。在感染区没有控制病害的经济上可行的生物学,化学或文化措施,这一事实导致人们寻找了涉及激活植物固有防御系统的替代策略。与双子叶植物相比,单子叶植物对系统获得性抗性(SAR)的机制了解较少。由于减毒或无毒病原体对植物的全身保护是典型的SAR反应,因此在香蕉中建立生物诱导的SAR模型有助于研究SAR对枯萎病的机理。本文描述了一种这样的模型,该模型使用不相容的Foc种族1在体外病理系统中诱导对Foc热带种族4的抗性。与在初次感染和挑战接种之间的时间间隔为10 d时SAR提供最高保护水平的观察结果一致,防御相关酶的活性例如苯丙氨酸氨裂合酶(PAL,EC 4.3.1.5),过氧化物酶(全身组织中的POD,EC 1.11.1.7),多酚氧化酶(PPO,EC 1.14.18.1)和超氧化物歧化酶(SOD,EC 1.15.1.1)也达到最高水平,比相应的组织高2.00-2.43倍在第十天进行控制。在第二叶片接种Foc种1后,香蕉幼苗根中的总水杨酸(SA)含量从约1增加到大于5 micro gg -1 FW。 MaNPR1A和MaNPR1B之后是PR-1和PR-3的第二次上调。尽管SA和茉莉酸(JA)/乙烯(ET)信号大部分是拮抗的,但在初次感染后,同时受不同信号途径调节的PR基因的系统表达同时上调,表明这两种途径均与SAR的激活有关。

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