Koch Martina, Vorwerk Sonja, Masur Clarissa, Sharifi-Sirchi Gholamreza, Olivieri Nicoletta, Schlaich Nikolaus L
RWTH Aachen University, Institut Bio III Pflanzenphysiologie, 52056 Aachen, Germany.
Plant J. 2006 Aug;47(4):629-39. doi: 10.1111/j.1365-313X.2006.02813.x. Epub 2006 Jul 19.
Using activation tagging in the Arabidopsis Col-0 rps2-101C background, we identified a mutant (FMO1-3D) that showed virtually no symptoms after inoculation with virulent Pseudomonas syringae pv. tomato DC3000 bacteria. The dominant, gain-of-function phenotype of the FMO1-3D mutant is due to over-expression of a class 3 flavin-containing mono-oxygenase (FMO). We recapitulated the FMO1-3D mutant phenotype in independent transgenic Col-0 lines over-expressing the FMO1 cDNA under the control of the 35S CaMV promoter. The increased basal resistance observed in the FMO1-3D mutant was also effective against the taxonomically unrelated downy mildew-causing pathogen Hyaloperonospora parasitica. By investigating the progeny from crosses of the FMO1-3D mutant with the NahG transgenic line, we showed that the enhanced basal resistance phenotype was dependent on the accumulation of salicylic acid. FMO1-3D plants showed wild-type resistant reactions after inoculation with avirulent bacteria, indicating that the R-gene-mediated defence physiology was not compromised by FMO1 over-expression. Transcripts of the class 3 FMO1 gene accumulated within 6 h after inoculation of wild-type Col-0 plants with avirulent Pst + avrRpt2 cells. Moreover, a T-DNA insertion into the FMO1 gene resulted in enhanced susceptibility to virulent Pseudomonas and Hyaloperonospora parasitica, suggesting that expression of the FMO1 gene is a hitherto undescribed component of the plant's resistance repertoire. We discuss the possibility that the FMO may participate in the detoxification of virulence factors produced by pathogens.
在拟南芥Col-0 rps2-101C背景下利用激活标签技术,我们鉴定出一个突变体(FMO1-3D),该突变体在用毒性强的丁香假单胞菌番茄致病变种DC3000细菌接种后几乎不表现出症状。FMO1-3D突变体的显性、功能获得型表型是由于3类含黄素单加氧酶(FMO)的过表达。我们在由35S CaMV启动子控制下过表达FMO1 cDNA的独立转基因Col-0株系中重现了FMO1-3D突变体表型。在FMO1-3D突变体中观察到的基础抗性增强对分类学上不相关的引起霜霉病的病原菌寄生霜霉也有效。通过研究FMO1-3D突变体与NahG转基因株系杂交的后代,我们表明增强的基础抗性表型依赖于水杨酸的积累。FMO1-3D植株在用无毒细菌接种后表现出野生型抗性反应,表明R基因介导的防御生理未因FMO1过表达而受损。在用无毒的丁香假单胞菌+avrRpt2细胞接种野生型Col-0植株后6小时内,3类FMO1基因的转录本积累。此外,FMO1基因中的T-DNA插入导致对毒性强的假单胞菌和寄生霜霉的易感性增强,表明FMO1基因的表达是植物抗性机制中一个迄今未被描述的组成部分。我们讨论了FMO可能参与病原体产生的毒力因子解毒的可能性。