Kiedrowski S, Kawalleck P, Hahlbrock K, Somssich I E, Dangl J L
Max-Delbrück-Laboratorium, Max-Planck-Institüt für Züchtungsforschung, Köln, Germany.
EMBO J. 1992 Dec;11(13):4677-84. doi: 10.1002/j.1460-2075.1992.tb05572.x.
We cloned and sequenced cDNAs encoded by a novel plant defense gene, ELI3, from parsley and Arabidopsis thaliana. The predicted product shares no homology to known sequences. ELI3 mRNA accumulates in A. thaliana leaves in response to challenge with phytopathogenic Pseudomonas syringae strains. The timing and magnitude of this response are dictated by the genetics of the plant-pathogen interaction being analyzed. During incompatible interactions, where resistance in the plant genotype Col-0 is dictated by the dominant RPM1 locus, ELI3 mRNA accumulates to high levels 5-10 h post-inoculation. This kinetic behavior is also generated by the presence of a cloned bacterial avirulence gene, in otherwise virulent bacteria, which triggers resistance mediated via RPM1 action. The phenotypic outcome is a hypersensitive resistance reaction visible 8-15 h post-infiltration. Thus, the induction kinetics of ELI3 mRNA accumulation are consistent with a functional role for the ELI3 gene product in establishing the resistant phenotype. In contrast, during compatible interactions with the susceptible plant genotype Nd-0, which is homozygous recessive at the rpm1 locus, ELI3 mRNA accumulates significantly only after 15 h. We show genetically that ELI3 activation is strictly dependent on the presence of dominant alleles at RPM1 using an assay generalizable to any pathogen induced plant defense phenomena.
我们从欧芹和拟南芥中克隆并测序了一个新的植物防御基因ELI3编码的cDNA。预测产物与已知序列无同源性。ELI3 mRNA在拟南芥叶片中积累,以响应植物致病性丁香假单胞菌菌株的攻击。这种反应的时间和强度由所分析的植物-病原体相互作用的遗传学决定。在不相容相互作用中,植物基因型Col-0中的抗性由显性RPM1基因座决定,ELI3 mRNA在接种后5-10小时积累到高水平。这种动力学行为也由克隆的细菌无毒基因的存在产生,在其他情况下为致病细菌,其触发通过RPM1作用介导的抗性。表型结果是在浸润后8-15小时可见的过敏抗性反应。因此,ELI3 mRNA积累的诱导动力学与ELI3基因产物在建立抗性表型中的功能作用一致。相比之下,在与易感植物基因型Nd-0的相容相互作用中,该基因型在rpm1基因座处是纯合隐性的,ELI3 mRNA仅在15小时后才显著积累。我们通过遗传学方法表明,使用一种可推广到任何病原体诱导的植物防御现象的检测方法,ELI3的激活严格依赖于RPM1处显性等位基因的存在。