CHARACTERIZATION OF AN ARABIDOPSIS MUTANT THAT IS NONRESPONSIVE TO INDUCERS OF SYSTEMIC ACQUIRED-RESISTANCE
CHARACTERIZATION OF AN ARABIDOPSIS MUTANT THAT IS NONRESPONSIVE TO INDUCERS OF SYSTEMIC ACQUIRED-RESISTANCE
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DOI：
10.1105/tpc.6.11.1583
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发表时间：
1994-11-01
期刊：
影响因子：
11.6
通讯作者：
DONG, XN
中科院分区：
文献类型：
--
作者：
CAO, H;BOWLING, SA;DONG, XN
系统获得抗性（SAR）是植物的一种普遍防御反应，其特征是病程相关基因（PR）的表达。SAR可以在对无毒病原体的过敏反应后或通过用水杨酸（SA）或2，6-二氯异烟酸（INA）处理而诱导。为了剖析SAR的信号转导途径，我们分离了一个拟南芥突变体，该突变体缺乏由拟南芥PR基因的5'非翻译区、β-1，3-葡聚糖酶（BGL 2）和β-葡萄糖醛酸酶（GUS）的编码区组成的SA-、INA-和病原体响应嵌合报告基因的表达。该突变体npr 1（PR基因的非表达者）携带一个单一的隐性突变，该突变也废除了其他PR基因的SAR响应性表达。虽然SA-，INA-或无毒病原体诱导的SAR保护野生型植物免受假单胞菌感染，但突变体不能通过用这些诱导剂预处理来保护。npr 1对SA、INA和无毒病原体在SAR诱导中的不敏感性表明这些诱导剂共享共同的信号转导途径。此外，在npr 1中，由有毒假单胞菌属病原体诱导的PR基因的局部表达被破坏，并且形成的损伤不那么局限。这些结果表明PR基因在预防病原体近端传播中的作用，除了它们在SAR中的作用。
Systemic acquired resistance (SAR) is a general defense response in plants that is characterized by the expression of pathogenesis-related (PR) genes. SAR can be induced after a hypersensitive response to an avirulent pathogen or by treatment with either salicylic acid (SA) or 2,6-dichloroisonicotinic acid (INA). To dissect the signal transduction pathway of SAR, we isolated an Arabidopsis mutant that lacks the expression of an SA-, INA-, and pathogen-responsive chimeric reporter gene composed of the 5' untranslated region of an Arabidopsis PR gene, beta-1,3-glucanase (BGL2), and the coding region of beta-glucuronidase (GUS). This mutant, npr1 (nonexpresser of PR genes), carries a single recessive mutation that abolishes the SAR-responsive expression of other PR genes as well. While SA-, INA-, or avirulent pathogen-induced SAR protects wild-type plants from Pseudomonas syringae infection, the mutant cannot be protected by pretreatment with these inducers. The insensitivity of npr1 to SA, INA, and avirulent pathogens in SAR induction indicates that these inducers share a common signal transduction pathway. Moreover, in npr1, the localized expression of PR genes induced by a virulent Pseudomonas pathogen is disrupted, and the lesion formed is less confined. These results suggest a role for PR genes in preventing the proximal spread of pathogens in addition to their suggested role in SAR.