果树火疫病研究进展

方茜,徐幼平,蔡新忠

Research progress of fire blight in fruit trees

Xi FANG,Youping XU,Xinzhong CAI

图2 植物与 E. amylovora 互作分子机制本图由Figdraw（http://www.figdraw.com）绘制。火疫病菌效应蛋白用不同颜色圆球表示，通过T3SS进入植物细胞质内；DspA/E和HrpN分别与LRR受体激酶DIPM1～4和跨膜蛋白HIPM互作，促进病害发生；Eop4/AvrRpt2EA切割MdRIN4，产生ACP3，活化R蛋白Mr5，激发ETI免疫；Eop1可能被FB_Mf12及FB_E12识别，激发抗病性；Eop2和Eop3的免疫识别机制尚不明确。

Fig. 2 Molecular mechanisms underlying plant-E. amylovora interactionsThe figure was drawn by Figdraw (http://www.figdraw.com). Erwinia amylovora effectors, which are indicated in colored circles, enter the plant cell through T3SS. DspA/E and HrpN physically interact with LRR receptor-like kinase DIPM1-4 and transmembrane protein HIPM, respectively, to promote disease development. Eop4/AvrRpt2EA cleaves MdRIN4 and produces ACP3, which activates the R protein Mr5 to trigger ETI. Eop1 might be recognized somehow by FB_Mf12 and FB_E12 to elicit ETI. The immune recognition of Eop2 and Eop3 remains unknown.