Signaling requirements and role of salicylic acid in HRT- and rrt-mediated resistance to turnip crinkle virus in Arabidopsis
Signaling requirements and role of salicylic acid in HRT- and rrt-mediated resistance to turnip crinkle virus in Arabidopsis
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DOI：
10.1111/j.1365-313x.2004.02241.x
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发表时间：
2004-12-01
期刊：
影响因子：
7.2
通讯作者：
Kachroo, P
中科院分区：
文献类型：
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作者：
Chandra-Shekara, AC;Navarre, D;Kachroo, P
芜菁皱缩病毒(TCV)接种于抗病的拟南芥Di-17生态型上引起过敏反应(HR)，伴随着病程相关(PR)基因表达的增加。以往的遗传分析表明，HR对TCV的抗性是由HRT决定的，HRT编码一个卷曲(CC)、核苷酸结合位点(NBS)和富含亮氨酸重复(LRR)类抗性(R)蛋白。与HR相反，对TCV的抗性既需要HRT，也需要第二个被称为RRT的座位上的隐性等位基因。在这里，我们证明了与大多数CC-NBS-LRR R基因不同，HRT/RRT介导的抗性依赖于EDS1，而不依赖于NDR1。抗性也与RAR1和SGT1无关。HRT/RRT介导的抗性在水杨酸(SA)含量降低的植物中受到损害，这是eds5、Pad4或sid2突变的结果。相比之下，HR不受eds1、eds5、Pad4、sid2、ndr1、rar1或sgt1b突变的影响。通过外源SA或SA类似物苯并(1，2，3)噻二唑-7-硫代酸(BTH)的应用，表达nahG转基因的SA缺乏的Di-17植株和含有eds1、eds5或sid2突变的突变体都恢复了对TCV的抗性。相反，SA/BTH处理未能提高Di-17与Col-0杂交的Hrt Pad4、Col-0或Hrt纯合子代的抗性。因此，HRT和PAD4是SA诱导抗性所必需的。如果存在HRT等位基因，外源供应的SA或由于SSI2突变而产生的高水平SA克服了RRT的抑制作用，并增强了对TCV的抵抗力。高水平的SA通过依赖PAD4的途径上调HRT的表达。由于高水平表达HRT的Col-0转基因株对TCV具有抗性，而表达中、低水平HRT的Col-0转基因株对TCV没有抗性，因此我们得出结论，SA通过上调HRT的表达来增强RRT背景下的抗性。这些数据表明，HRT-TCV相互作用不能产生稳定的抗性表型所需的足够数量的SA，RRT的存在可能纠正这一不足。
Inoculation of turnip crinkle virus (TCV) on the resistant Arabidopsis ecotype Di-17 elicits a hypersensitive response (HR), which is accompanied by increased expression of pathogenesis-related (PR) genes. Previous genetic analyses revealed that the HR to TCV is conferred by HRT, which encodes a coiled-coil (CC), nucleotide-binding site (NBS) and leucine-rich repeat (LRR) class resistance (R) protein. In contrast to the HR, resistance to TCV requires both HRT and a recessive allele at a second locus designated rrt. Here, we demonstrate that unlike most CC-NBS-LRR R genes, HRT/rrt-mediated resistance is dependent on EDS1 and independent of NDR1. Resistance is also independent of RAR1 and SGT1. HRT/rrt-mediated resistance is compromised in plants with reduced salicylic acid (SA) content as a consequence of mutations eds5, pad4, or sid2. By contrast, HR is not affected by mutations in eds1, eds5, pad4, sid2, ndr1, rar1, or sgt1b. Resistance to TCV is restored in both SA-deficient Di-17 plants expressing the nahG transgene and mutants containing the eds1, eds5, or sid2 mutations by exogenous application of SA or the SA analog benzo(1,2,3)thiadiazole-7-carbothioic acid (BTH). In contrast, SA/BTH treatment failed to enhance resistance in HRT pad4, Col-0, or hrt homozygous progeny of a cross between Di-17 and Col-0. Thus, HRT and PAD4 are required for SA-induced resistance. Exogenously supplied SA or high endogenous levels of SA, due to the ssi2 mutation, overcame the suppressive effects of RRT and enhanced resistance to TCV, provided the HRT allele was present. High levels of SA upregulate HRT expression via a PAD4-dependent pathway. As Col-0 transgenic lines expressing high levels of HRT were resistant to TCV, but lines expressing moderate to low levels of HRT were not, we conclude that SA enhances resistance in the RRT background by upregulating HRT expression. These data suggest that the HRT-TCV interaction is unable to generate sufficient amounts of SA required for a stable resistance phenotype, and the presence of rrt possibly corrects this deficiency.