Plant Physiol. Journal of Pharmacology and Experimental Therapeutics
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Published on March 16, 2007; 10.1104/pp.106.095299

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Received December 27, 2006
Accepted March 10, 2007

Genetic Interactions of TGA Transcription Factors in the regulation of Pathogenesis Related Genes and Disease Resistance in Arabidopsis thaliana

Meenu Kesarwani *, Jungmin Yoo , and Xinnian Dong

Department of Biology, Box 90338, Duke University, Durham, North Carolina 27708, USA

* Corresponding author; email: kmeenu{at}molbio.mgh.harvard.edu.

TGA transcription factors are implicated as regulators of pathogenesis-related (PR) genes because of their physical interaction with the known positive regulator, NPR1. A triple knockout mutant tga2-1 tga5-1 tga6-1 was shown previously to be defective in the induction of PR genes and systemic acquired resistance (SAR), confirming their role in disease resistance. However, the contributions of individual TGA factors have been difficult to discern because of functional redundancy among these factors as well as possible dual functions for some single factors. In the present study, we characterized six TGA factors by reverse genetics. We show that TGA3 is required for both basal and 2,6-dichloroisonicotinic acid (INA)-induced transcription of PR genes. The tga3-1 mutants were found to be defective in basal pathogen resistance, while the induced resistance was unaffected. TGA1 and TGA4 play partially redundant roles in regulation of basal resistance, having only moderate effects on PR gene expression. Additionally, an activation-tagged mutant of TGA6 was able to increase basal as well as induced expression of PR-1, demonstrating a positive role for TGA6 on PR gene expression. In contrast, TGA2 has a repressor activity on PR gene expression even though it can act as a positive regulator in the tga5-1 tga6-1 null mutant background. Finally we examined the genetic interaction between tga2-2 and the suppressor of npr1 inducible 1 (sni1-1). TGA2's repressor activity overlaps with SNI1, because the tga2-2 sni1-1 double mutant shows a synergistic effect on PR gene expression.




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