Stevens C, Bennett M A, Athanassopoulos E, Tsiamis G, Taylor J D, Mansfield J W
Department of Biological Sciences, Wye College, University of London, Ashford, UK.
Mol Microbiol. 1998 Jul;29(1):165-77. doi: 10.1046/j.1365-2958.1998.00918.x.
The bean halo blight pathogen, Pseudomonas syringae pv. phaseolicola (Psph), is differentiated into nine races based on the presence or absence of five avirulence (avr) genes in the bacterium, which interact with corresponding resistance genes. R1-R5, in Phaseolus vulgaris. The resistance gene R2 is matched by avrPphE, which is located adjacent to the cluster of hrp genes that are required for pathogenicity of Psph. Although only races 2, 4, 5 and 7 are avirulent on cultivars with R2 (inducing the hypersensitive response; HR), homologues of avrPphE are present in all races of Psph. DNA sequencing of avrPphE alleles from races of Psph has demonstrated two routes to virulence: via single basepair changes conferring amino acid substitutions in races 1, 3, 6 and 9 and an insertion of 104bp in the allele in race 8. We have demonstrated that these base changes are responsible for the difference between virulence and avirulence by generating transconjugants of a virulent race harbouring plasmids expressing the various alleles of avrPphE. Agrobacterium tumefaciens-directed expression of avrPphE from race 4 in bean leaves induced the HR in a resistance gene-specific manner, suggesting that the AvrPphE protein is alone required for HR induction and is recognized within the plant cell. The allele from race 6, which is inactive if expressed in Psph, elicited a weak HR if expressed in planta, whereas the allele from race 1 did not. Our results suggest that the affinity of interaction between AvrPphE homologues and an unknown plant receptor mediates the severity of the plant's response. Mutation of avrPphE alleles did not affect the ability to colonize bean from a low level of inoculum. The avirulence gene avrPphB, which matches the R3 resistance gene, also caused a gene-specific HR following expression in the plant after delivery by A. tumefaciens.
菜豆晕疫病病原菌丁香假单胞菌菜豆致病变种（Psph），根据细菌中五个无毒（avr）基因的有无分为九个小种，这些基因与菜豆中的相应抗性基因R1 - R5相互作用。抗性基因R2与avrPphE匹配，avrPphE位于Psph致病性所需的hrp基因簇附近。虽然只有小种2、4、5和7对含有R2的品种无毒（诱导超敏反应；HR），但avrPphE的同源物存在于Psph的所有小种中。对Psph小种的avrPphE等位基因进行DNA测序表明，有两条产生毒性的途径：小种1、3、6和9通过单碱基对变化导致氨基酸替换，小种8的等位基因中插入了104bp。我们通过构建携带表达avrPphE各种等位基因质粒的毒性小种的转接合子，证明了这些碱基变化是毒性和无毒之间差异的原因。根癌农杆菌介导在菜豆叶片中表达小种4的avrPphE以抗性基因特异性方式诱导了HR，这表明AvrPphE蛋白单独即可诱导HR，并且在植物细胞内被识别。小种6的等位基因如果在Psph中表达则无活性，但在植物中表达时会引发微弱的HR，而小种1的等位基因则不会。我们的结果表明，AvrPphE同源物与未知植物受体之间相互作用的亲和力介导了植物反应的强度。avrPphE等位基因的突变不影响从低接种量定殖菜豆的能力。与R3抗性基因匹配的无毒基因avrPphB在通过根癌农杆菌传递后在植物中表达时也会引起基因特异性HR。
