Genetic interactions of TGA transcription factors in the regulation of pathogenesis-related genes and disease resistance in Arabidopsis.

Published

Journal Article

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.

Full Text

Duke Authors

Cited Authors

  • Kesarwani, M; Yoo, J; Dong, X

Published Date

  • May 2007

Published In

Volume / Issue

  • 144 / 1

Start / End Page

  • 336 - 346

PubMed ID

  • 17369431

Pubmed Central ID

  • 17369431

Electronic International Standard Serial Number (EISSN)

  • 1532-2548

International Standard Serial Number (ISSN)

  • 0032-0889

Digital Object Identifier (DOI)

  • 10.1104/pp.106.095299

Language

  • eng