de Wit P J, Joosten M H, Honée G, Wubben J P, van den Ackerveken G F, van den Broek H W
Wageningen Agricultural University, Department of Phytopathology, The Netherlands.
Antonie Van Leeuwenhoek. 1994;65(3):257-62. doi: 10.1007/BF00871954.
Host genotype specificity in interactions between biotrophic fungal pathogens and plants in most cases complies with the gene-for-gene model. Success or failure of infection is determined by absence or presence of complementary genes, avirulence and resistance genes, in the pathogen and the host plant, respectively. Resistance, expressed by the induction of a hypersensitive response followed by other defence responses in the host, is envisaged to be based on recognition of the pathogen, mediated through direct interaction between products of avirulence genes of the pathogen (the so-called race-specific elicitors) and receptors in the host plant, the putative products of resistance genes. The interaction between the biotrophic fungus Cladosporium fulvum and its only host tomato is a model system to study fungus-plant gene-for-gene relationships. Here we report on isolation, characterization and biological function of putative pathogenicity factors ECP1 and ECP2 and the race-specific elicitors AVR4 and AVR9 of C. fulvum and cloning and regulation of their encoding genes. Disruption of ecp1 and ecp2 genes has no clear effect on pathogenicity of C. fulvum. Disruption of the avr9 gene, which codes for the race-specific 28 amino acid AVR9 elicitor, in wild type avirulent races, leads to virulence on tomato genotypes carrying the complementary resistance gene Cf9. The avirulence gene avr4 encodes a 105 amino acid race-specific elicitor. A single basepair change in the avirulence gene avr4 leads to virulence on tomato genotypes carrying the Cf4 resistance gene.
在大多数情况下，活体营养型真菌病原体与植物之间相互作用的宿主基因型特异性符合基因对基因模型。感染的成功或失败分别由病原体和宿主植物中互补基因（无毒基因和抗性基因）的缺失或存在决定。宿主通过诱导超敏反应继而引发其他防御反应来表达抗性，这种抗性被认为是基于对病原体的识别，由病原体无毒基因的产物（所谓的小种特异性激发子）与宿主植物中的受体（抗性基因的推定产物）之间的直接相互作用介导。活体营养型真菌番茄叶霉及其唯一宿主番茄之间的相互作用是研究真菌 - 植物基因对基因关系的模型系统。在此，我们报道了番茄叶霉推定致病因子ECP1和ECP2以及小种特异性激发子AVR4和AVR9的分离、表征和生物学功能，以及它们编码基因的克隆和调控。ecp1和ecp2基因的破坏对番茄叶霉的致病性没有明显影响。在野生型无毒小种中，编码28个氨基酸的小种特异性激发子AVR9的avr9基因被破坏，会导致对携带互补抗性基因Cf9的番茄基因型产生毒性。无毒基因avr4编码一个105个氨基酸的小种特异性激发子。无毒基因avr4中的一个碱基对变化会导致对携带Cf4抗性基因的番茄基因型产生毒性。
