Takahashi Hideki, Kanayama Yoshinori, Zheng Ming Shu, Kusano Tomonobu, Hase Shu, Ikegami Masato, Shah Jyoti
Department of Life Science, Graduate School of Agricultural Science, Tohoku University, 1-1 Tsutsumidori-Amamiyamachi, Aoba-ku, Sendai, 981-8555 Japan.
Plant Cell Physiol. 2004 Jun;45(6):803-9. doi: 10.1093/pcp/pch085.
Gene-for-gene resistance to a yellow strain of cucumber mosaic virus [CMV(Y)] is conferred by the dominant RESISTANCE to CMV(Y) (RCY1) allele in the Arabidopsis thaliana ecotype C24. RCY1-conferred resistance to CMV(Y) and expression of the Pathogenesis-related 1 (PR-1) and PR-5 genes are partially compromised by the eds5 mutation and the nahG transgene that block accumulation of salicylic acid (SA). In contrast, the RCY1-conferred resistance to CMV(Y) is not affected by the jasmonic acid (JA)-insensitive coi1 and jar1 mutations. Interestingly, we report here that in contrast to the eds5 RCY1 plant, the eds5 coi1 RCY1 double-mutant plant exhibited a higher level of resistance to CMV(Y). Presence of the coi1 mutant allele also restored the CMV(Y)-activated expression of the PR-1 and PR-5 gene in the eds5 coi1 RCY1 plant. In contrast to the PR-1 and PR-5 genes, expression of the JA-dependent PLANT DEFENSIN 1.2 (PDF1.2) and HEVEIN-LIKE PROTEIN (HEL) genes was elevated in the CMV(Y)-inoculated leaves of the eds5 RCY1 plant, but not in the virus-inoculated leaves of the wild-type RCY1 and coi1 RCY1 plants. We propose that antagonistic interactions between the SA and JA signaling mechanisms modulate defense gene expression and the activation of RCY1-conferred gene-for-gene resistance to CMV(Y).
拟南芥生态型C24中的显性抗黄瓜花叶病毒黄色株系[CMV(Y)]基因（RCY1）赋予了对CMV(Y)的基因对基因抗性。EDS5突变和nahG转基因会阻断水杨酸（SA）的积累，从而部分削弱了RCY1介导的对CMV(Y)的抗性以及病程相关蛋白1（PR-1）和PR-5基因的表达。相比之下，RCY1介导的对CMV(Y)的抗性不受茉莉酸（JA）不敏感的coi1和jar1突变的影响。有趣的是，我们在此报告，与eds5 RCY1植株不同，eds5 coi1 RCY1双突变植株对CMV(Y)表现出更高水平的抗性。coi1突变等位基因的存在还恢复了eds5 coi1 RCY1植株中CMV(Y)激活的PR-1和PR-5基因的表达。与PR-1和PR-5基因不同，JA依赖的植物防御素1.2（PDF1.2）和类橡胶素蛋白（HEL）基因在eds5 RCY1植株接种CMV(Y)的叶片中表达升高，但在野生型RCY1和coi1 RCY1植株接种病毒的叶片中未升高。我们提出，SA和JA信号传导机制之间的拮抗相互作用调节防御基因的表达以及RCY1介导的对CMV(Y)的基因对基因抗性的激活。
