山荆子MbLRK10L1.1基因正调控腐烂病抗性  

Gene MbLRK10L1.1 Positively RegulatesValsa Canker in Malus baccata

作　　者：鲁远 冒霞 王超 孙娥 郑艳 左存武[1] LU Yuan;MAO Xia;WANG Chao;SUN E;ZHENG Yan and ZUO Cunwu(College of Horticulture,Gansu Agricultural University,Lanzhou 730070,China)

机构地区：[1]甘肃农业大学园艺学院,兰州730070

出　　处：《西北农业学报》2024年第3期552-561,共10页Acta Agriculturae Boreali-occidentalis Sinica

基　　金：甘肃省科技特派团专项(22CX8NA026);甘肃省科技重大专项(22ZD6NA045)。

摘　　要：此前从东北山荆子(Malus baccata)中发现可能参与腐烂病信号响应的WAK基因 MbLRK10L1.1,在此基础上,拟结合生物信息学分析、表达分析和功能验证研究其在腐烂病抗性中的作用机制。结果表明, MbLRK10L1.1响应Valsa mali(Vm)信号,并且在瞬时表达 MbLRK10L1.1后,‘烟富6号’果实表面病斑扩散速率明显减小, FRK1(Flg22-induced Receptor-like Kinase 1)、TaNOX(Triticum aestivum NADPH oxidase)、 EDS1(Enhanced disease susceptibility 1)等相关抗病基因均有不同程度的上调表达。表明 MbLRK10L1.1可通过JA、SA、SAR以及PTI等途径正调控果实对腐烂病菌的抗性。Valsa canker caused by Valsa mali(Vm)is a prevalent fungal disease affecting the apple industry.Wall-associated kinases(WAKs)play an important role in cell proliferation,growth and development,pathogen resistance and other physiological responses in plants.In the previous work,we identified the WAK genes,MbLRK10L1.1,from Malus baccata,which is potentially associated with the response to Vm infection.On this basis,this study integrated bioinformatics analysis,expression analysis and functional validation to elucidate the molecular mechanism underlying the involvement of MbLRK10L1.1 in the response to Vm.The results showed that MbLRK10L1.1 responded to the Vm signaling,and overexpression of MbLRK10L1.1 significantly reduced the rate of lesion spread on the fruit surface.The upregulation of disease resistance-related genes such as FRK1(Flg22-induced Receptor-like Kinase 1),TaNOX(Triticum aestivum NADPH Oxidase),EDS1(Enhanced Disease Susceptibility 1)and others were observed.The above results indicated that the gene(MbLRK10L1.1)could positively regulate the resistance of apple to the Valsa canker through JA,SA,SAR,and PTI pathways.

关 键 词：腐烂病(Valsa canker) WAK基因 瞬时表达标记基因 

分 类 号：S661.1[农业科学—果树学]