Characterization of a salicylic acid-insensitive mutant (sai1) of Arabidopsis thaliana, identified in a selective screen utilizing the SA-inducible expression of the tms2 gene
Characterization of a salicylic acid-insensitive mutant (sai1) of Arabidopsis thaliana, identified in a selective screen utilizing the SA-inducible expression of the tms2 gene
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DOI：
10.1094/mpmi.1997.10.1.69
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发表时间：
1997-01-01
影响因子：
3.5
通讯作者：
Klessig, DF
中科院分区：
文献类型：
--
作者：
Shah, J;Tsui, F;Klessig, DF
水杨酸（Salicylic acid， SA）在许多植物抵抗病原菌入侵的过程中起着重要的信号作用。内源性SA水平的增加与过敏反应和全身获得性耐药（SAR）有关。SA还能诱导一部分致病相关（PR）基因的表达。然而，对抗性反应期间SA积累后发生的事件所知相对较少。为了鉴定SA信号转导通路成分的突变，我们在拟南芥中开发了一种遗传筛选方法，利用农杆菌tms2基因作为反选择标记。sa诱导烟草PR-1a启动子表达的tms2基因对α -萘乙酰胺（α - nam）敏感，导致转基因拟南芥幼苗发芽时根系生长受到抑制。从这个PR-1a:tms2转基因系中选择了根生长对α - nam不敏感的突变体，期望一个子集将缺乏SA下游的调节成分。这样鉴定的sail突变体既不表达PR-1a:tms2转基因，也不表达内源拟南芥PR-1、PR-2和PR-5基因。这些基因在sail中也没有被2,6-二氯异烟碱酸（INA）或苯并噻二唑（BTH）这两种SAR的化学诱诱剂诱导。正如预期的SA下游突变一样，sail植物在受到无毒病原体感染时积累SA及其糖苷，并且比野生型亲本更容易受到这种无毒病原体的感染。sail是npr1的等位基因，npr1是一种先前发现的sa非诱导突变。非诱导性sail突变的隐性性质表明，野生型SA11基因在SA信号转导途径中起着积极的调节作用。
Salicylic acid (SA) plays an important signaling role in the resistance of many plants to pathogen invasion. Increases in endogenous SA levels have been associated with the hypersensitive response as well as systemic acquired resistance (SAR). SA also induces the expression of a subset of the pathogenesis-related (PR) genes. However, relatively little is known about the events occurring subsequent to SA accumulation during a resistance response. In order to identify mutations in components of the SA signal transduction pathway, we have developed a genetic screen in Arabidopsis thaliana that utilizes the Agrobacterium tumefaciens tms2 gene as a counter-selectable marker. SA-inducible expression of the tms2 gene from the tobacco PR-1a promoter confers sensitivity to a-naphthalene acetamide (alpha-NAM), resulting in inhibition of root growth in germinating transgenic Arabidopsis seedlings. Mutants in which root growth is insensitive to alpha-NAM have been selected from this PR-1a:tms2 transgenic line with the expectation that a subset will lack a regulatory component downstream of SA. The sail mutant so identified expressed neither the PR-1a:tms2 transgene nor the endogenous Arabidopsis PR-1, PR-2, and PR-5 genes in response to SA. These genes also were not induced in sail by 2,6-dichloroisonicotinic acid (INA) or benzothiadiazole (BTH), two chemical inducers of SAR. As expected of a mutation acting downstream of SA, sail plants accumulate SA and its glucoside in response to infection with an avirulent pathogen and are more susceptible to this avirulent pathogen than the wild-type parent. sail is allelic to npr1, a previously identified SA-noninducible mutation. The recessive nature of the noninducible sail mutation suggests that the wild-type SA11 gene acts as a positive regulator in the SA signal transduction pathway.