Antagonistic interactions between the SA and JA signaling pathways in Arabidopsis modulate expression of defense genes and gene-for-gene resistance to cucumber mosaic virus

Antagonistic interactions between the SA and JA signaling pathways in Arabidopsis modulate expression of defense genes and gene-for-gene resistance to cucumber mosaic virus
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DOI:
10.1093/pcp/pch085
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发表时间:
2004-06-01
影响因子:
4.9
通讯作者:
Shah, J
Shah, J
中科院分区:
生物学2区
文献类型:
--
作者:
Takahashi, H;Kanayama, Y;Shah, J

文献摘要

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对黄瓜花叶病毒(CMV(Y))黄株的基因对基因抗性是由拟南芥(Arabidopsis thaliana) C24型中对CMV(Y) (RCY1)的显性等位基因赋予的。rcy1对CMV(Y)的抗性以及致病相关1 (PR-1)和PR-5基因的表达部分受到eds5突变和nahG转基因的损害,该基因可阻断水杨酸(SA)的积累。相比之下,rcy1对CMNI(Y)的抗性不受茉莉酸(JA)不敏感线圈和jar1突变的影响。有趣的是,我们在这里报道,与eds5 RCY1植株相比,eds5线圈RCY1双突变植株对CMV(Y)表现出更高水平的抗性。在eds5线圈RCY1植株中,线圈突变等位基因的存在也恢复了CMV(Y)激活的PR-1和PR-5基因的表达。与pr - 1和PR-5基因相比,ja依赖性植物防御素1.2 (PDF1.2)和HE静脉样蛋白(HEL)基因在CMV(Y)接种的eds5 RCY1植株叶片中表达升高,而在野生型RCY1和卷曲型RCY1植株的病毒接种叶片中表达升高。我们提出,SA和JA信号机制之间的拮抗相互作用调节了防御基因的表达和rcy1赋予的对CMV(Y)的基因对基因抗性的激活。
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 CMNI(Y) is not affected by the jasmonic acid (JA)-insensitive coil and jar1 mutations. Interestingly, we report here that in contrast to the eds5 RCY1 plant, the eds5 coil RCY1 double-mutant plant exhibited a higher level of resistance to CMV(Y). Presence of the coil mutant allele also restored the CMV(Y)-activated expression of the PR-1 and PR-5 gene in the eds5 coil RCY1 plant. In contrast to the PR-I and PR-5 genes, expression of the JA-dependent PLANT DEFENSIN 1.2 (PDF1.2) and HE VEIN-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 coil 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).