Institute of Molecular Biology and Biotechnology, Foundation for Research and Technology, Hellas, Crete, Greece.
Mol Plant Microbe Interact. 2011 Aug;24(8):907-17. doi: 10.1094/MPMI-01-11-0010.
Plant- and animal-pathogenic bacteria deploy a variable arsenal of type III effector proteins (T3EP) to manipulate host defense. Specific biochemical functions and molecular or subcellular targets have been demonstrated or proposed for a growing number of T3EP but remain unknown for the majority of them. Here, we show that transient expression of genes coding certain bacterial T3EP (HopAB1, HopX1, and HopF2), which did not elicit hypersensitive response (HR) in transgenic green fluorescent protein (GFP) Nicotiana benthamiana 16C line, enhanced the sense post-transcriptional gene silencing (S-PTGS) triggered by agrodelivery of a GFP-expressing cassette and the silencing enhancement could be blocked by two well-known viral silencing suppressors. Further analysis using genetic truncations and site-directed mutations showed that the receptor recognition domains of HopAB1 and HopX1 are not involved in enhancing silencing. Our studies provide new evidence that phytobacterial pathogen T3EP manipulate the plant small interfering RNA pathways by enhancing silencing efficiency in the absence of effector-triggered immunity signaling and suggest that phytopathogenic bacterial effectors affect host RNA silencing in yet other ways than previously described.
植物和动物病原细菌利用可变的 III 型效应蛋白(T3EP)武器库来操纵宿主防御。越来越多的 T3EP 的特定生化功能和分子或亚细胞靶标已经得到证实或提出,但大多数 T3EP 的靶标仍然未知。在这里,我们表明,瞬时表达编码某些细菌 T3EP(HopAB1、HopX1 和 HopF2)的基因,这些基因在转绿色荧光蛋白(GFP)拟南芥 16C 系中不会引发过敏反应(HR),增强了由 GFP 表达盒农杆菌介导的感测转录后基因沉默(S-PTGS),而沉默增强可以被两种已知的病毒沉默抑制剂阻断。进一步的遗传截短和定点突变分析表明,HopAB1 和 HopX1 的受体识别结构域不参与增强沉默。我们的研究提供了新的证据,表明植物病原菌 T3EP 通过在没有效应触发免疫信号的情况下增强沉默效率来操纵植物小干扰 RNA 途径,并表明植物病原细菌效应物以以前未描述的其他方式影响宿主 RNA 沉默。