Malamy J., Hennig J., Klessig D. F.
Waksman Institute, Rutgers, The State University of New Jersey, P.O. Box 759, Piscataway, New Jersey 08855.
Plant Cell. 1992 Mar;4(3):359-366. doi: 10.1105/tpc.4.3.359.
Increases in endogenous salicylic acid (SA) levels and induction of several families of pathogenesis-related genes (PR-1 through PR-5) occur during the resistance response of tobacco to tobacco mosaic virus infection. We found that at temperatures that prevent the induction of PR genes and resistance, the increases in SA levels were eliminated. The addition of exogenous SA to infected plants at these temperatures was sufficient to induce the PR genes but not the hypersensitive response. However, when the resistance response was restored by shifting infected plants to permissive temperatures, SA levels increased dramatically and preceded PR-1 gene expression and necrotic lesion formation associated with resistance. SA was also found in a conjugated form whose levels increased in parallel with the free SA levels. The majority of the conjugates appeared to be SA glucosides. The same glucoside was formed when plants were supplied with exogenous SA. These results provide further evidence that endogenous SA signals the induction of certain defense responses and suggests additional complexity in the modulation of this signal.
在烟草对烟草花叶病毒感染的抗性反应过程中，内源性水杨酸（SA）水平升高，并且多种病程相关基因家族（PR-1至PR-5）被诱导。我们发现，在阻止PR基因诱导和抗性产生的温度下，SA水平的升高被消除。在这些温度下，向受感染植物添加外源SA足以诱导PR基因，但不能诱导超敏反应。然而，当通过将受感染植物转移到适宜温度来恢复抗性反应时，SA水平急剧增加，并先于与抗性相关的PR-1基因表达和坏死病斑形成。还发现SA以共轭形式存在，其水平与游离SA水平平行增加。大多数共轭物似乎是SA糖苷。当给植物提供外源SA时，会形成相同的糖苷。这些结果进一步证明内源性SA为某些防御反应的诱导发出信号，并表明该信号调节存在额外的复杂性。
