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.
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 alpha-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 sai1 by 2,6-dichloroisonicotinic acid (INA) or benzothiadiazole (BTH), two chemical inducers of SAR. As expected of a mutation acting downstream of SA, sai1 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. sai1 is allelic to npr1, a previously identified SA-noninducible mutation. The recessive nature of the noninducible sai1 mutation suggests that the wild-type SAI1 gene acts as a positive regulator in the SA signal transduction pathway.
Shah
J
J
Waksman Institute, Rutgers, State University of New Jersey, Piscataway 08855, USA.
Tsui
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Klessig
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D000581:Amidohydrolases / Q000096:biosynthesis*; D017360:Arabidopsis / Q000235:genetics* / Q000502:physiology*; D002678:Chimera; D003433:Crosses, Genetic; D004198:Disease Susceptibility; D004790:Enzyme Induction; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005020:Ethyl Methanesulfonate; D018506:Gene Expression Regulation, Plant / Q000187:drug effects; D017343:Genes, Plant / Q000187:drug effects; D005816:Genetic Complementation Test; D007539:Isonicotinic Acids / Q000494:pharmacology; D016296:Mutagenesis; D016254:Mutagenesis, Insertional; D009280:Naphthaleneacetic Acids / Q000494:pharmacology; D010935:Plant Diseases; D030821:Plants, Genetically Modified; D010947:Plants, Toxic; D011549:Pseudomonas / Q000472:pathogenicity; D012459:Salicylates / Q000494:pharmacology*; D020156:Salicylic Acid; D013830:Thiadiazoles / Q000494:pharmacology; D014026:Nicotiana; D014170:Transformation, Genetic; D014774:Virulence
D004791:Enzyme Inhibitors; D007539:Isonicotinic Acids; D009280:Naphthaleneacetic Acids; D012459:Salicylates; D013830:Thiadiazoles; C025234:naphthaleneacetamide; C015700:benzo-1,2,3-thiadiazole; C077261:2,6-dichloroisonicotinic acid; D005020:Ethyl Methanesulfonate; D000581:Amidohydrolases; C058772:indole-3-acetamide hydrolase; D020156:Salicylic Acid