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First published online March 16, 2007; 10.1104/pp.106.095299 Plant Physiology 144:336-346 (2007) © 2007 American Society of Plant Biologists
Genetic Interactions of TGA Transcription Factors in the Regulation of Pathogenesis-Related Genes and Disease Resistance in Arabidopsis1,[W]Department of Biology, Duke University, Durham, North Carolina 27708
TGA transcription factors are implicated as regulators of pathogenesis-related (PR) genes because of their physical interaction with the known positive regulator, nonexpresser of PR gene1 (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, 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 this study, we characterized six TGA factors by reverse genetics. We show that TGA3 is required for both basal and 2,6-dichloroisonicotinic acid-induced transcription of PR genes. The tga3-1 mutants were found to be defective in basal pathogen resistance, whereas 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 PR1, demonstrating a positive role for TGA6 on PR gene expression. In contrast, TGA2 has 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 suppressor of npr1 inducible1 (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.
1 This work was supported by the National Research Initiative of the U.S. Department of Agriculture Cooperative State Research, Education, and Extension Service (grant no. 200300981); by the National Science Foundation (grant no. 0090887); and by Monsanto (grant to X.D.). The author responsible for distribution of materials integral to the findings presented in this article in accordance with the policy described in the Instructions for Authors (www.plantphysiol.org) is: Xinnian Dong (xdong{at}duke.edu). [W] The online version of this article contains Web-only data. www.plantphysiol.org/cgi/doi/10.1104/pp.106.095299 * Corresponding author; e-mail kmeenu{at}molbio.mgh.harvard.edu; fax 6177248558. Received December 27, 2006; accepted March 10, 2007; published March 16, 2007. This article has been cited by other articles:
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