H2O2和MAPK参与NO诱导的采后芒果抗炭疽病的作用机制研究

Fungal decay is a major cause of postharvest losses in fresh fruits. Although utilization of synthetic chemical fungicides is still the main method to control postharvest diseases, increasing concerns about fungicide residues on development of resistant biotypes of pathogens, as well as public concern over food and environment safety, have created interest in new strategies for postharvest disease management. Induction of resistance to pathogens in postharvested fruits using elicitors is becoming a promising approach for controlling postharvest diseases as an alternative to fungicides. Nitric oxide (NO) is an important signaling molecule, existing widely in organism. NO can induce defense responses to pathogens in plant. It has been known that multiple signaling molecules are involved in the process of NO-inducible defense responses to pathogens in plant. Both hydrogen peroxide (H2O2) and mitogen-activated protein kinase (MAPK) are involved in plant resistance to pathogens. However, little information is available on the mechanisms of hydrogen peroxide (H2O2) and mitogen-activated protein kinase (MAPK) involved in the process of NO-inducible defense responses to pathogens in plant. In our previous work, we have found that pre-storage application of NO can decrease disease incidence and suppress postharvest deterioration of mango fruit. On the basis of these results, the present project will focus on the response of H2O2 and MAPK during NO-induced anthracnose resistance in postharvested mango by means of pharmacological, physiological and biochemical, molecular biology. The results will help us to better reveal signal transduction pathway and action mechanism of H2O2 and MAPK in NO-induced disease resistance. It also provides a theoretical basis for further clear the role and signal transduction mechanism of NO in the control of postharvest diseases. In addition, the results provide a theoretical basis and practice guidance for further use the components of signal transduction to enhance resistance to pathogens in postharvested fruits.

病原菌侵染是导致采后新鲜水果腐烂的主要原因，而大量化学杀菌剂的使用正威胁着生态环境和人类健康。利用诱抗剂替代化学杀菌剂提高果实抗病性是防治果实采后病害的一个重要策略。NO是一种广泛存在于生物体内的信号分子，其诱导植物的抗病反应过程中需要多级信号分子的参与。H2O2和MAPK均可参与植物的抗病反应，但关于其在NO诱导果实采后抗病性方面的机理尚不明确。本项目在明确NO能够降低芒果采后炭疽病害发生的基础上，通过药理学、生理生化和分子生物学等研究手段，着重研究H2O2和MAPK参与NO诱导芒果采后炭疽病抗性的响应，旨在揭示H2O2和MAPK在NO抗病诱导中信号传导途径和作用机制，为进一步明确NO在芒果采后病害控制中的作用和抗病信号转导机理提供了理论依据，也为今后进一步利用信号转导组分增强果实采后抗病能力提供了理论基础和实践指导。

病害是导致采后果实腐烂的重要原因，其中炭疽病害是导致芒果采后损失的重要原因之一。一氧化氮(NO)是一种广泛存在于生物体内的信号分子，其诱导植物的抗病反应过程中需要多级信号分子的参与。过氧化氢(H2O2)和促分裂原活化蛋白激酶(MAPK)也常常作为细胞信使或信号分子参与植物的抗病反应。本项目以采后芒果果实为实验材料，探讨外源NO诱导采后芒果对炭疽病菌侵染的抗性的响应、以及H2O2和MAPK在NO诱导采后芒果果实抗病途径中的作用和机制。研究结果表明：在炭疽病原菌C. gloeosporioides侵染的情况下，SNP处理可以明显降低接种芒果果实发病率，抑制病斑的扩展，减轻果实的发病程度；SNP处理在提高芒果果实对接种炭疽病菌抗病性的过程中伴随有NO和H2O2含量以及MAPK活性的明显增加；果实抗病过程中NOS途径是NO产生的主要途径；SNP处理能诱导接种果实抗病酶活性的提高和抗病物质的积累；DPI和U0126均可削弱NO在提高芒果炭疽病抗性中的作用，表现为发病率和发病程度加重，抗病物质含量、抗病酶活性和关键基因表达下降，说明H2O2和MAPK在NO提高芒果炭疽病抗性中起着重要作用。进一步分析表明，DPI处理并未影响NO爆发，但却抑制了MAPK活性，而U0126处理对NO和H2O2爆发均未产生明显影响，这表明在芒果和C. gloeosporioides互作过程中，NO位于H2O2和MAPK信号通路的上游位置，而MAPK级联系统位于H2O2信号通路的下游。本研究结果为从信号途径方面揭示NO在芒果采后病害控制中的作用和机理提供了理论依据。