First published online October 23, 2003; 10.1105/tpc.014894
The Plant Cell, Vol. 15, 2647-2653, November 2003,
www.plantcell.org ©2003, American Society of Plant Biologists
Knockout Analysis of Arabidopsis Transcription Factors TGA2, TGA5, and TGA6 Reveals Their Redundant and Essential Roles in Systemic Acquired Resistance
Yuelin Zhang1,a,
Mark J. Tessaroa,
Michael Lassnerb and
Xin Lia
a Biotechnology Laboratory, University of British Columbia, Vancouver, British Columbia V6T 1Z3, Canada
b Maxygen, Inc., Redwood City, California 94063
1 To whom correspondence should be addressed. E-mail yuelin{at}interchange.ubc.ca; fax 1-604-822-6089
Arabidopsis nonexpresser of pathogenesis-related (PR) genes (NPR1) is the sole positive regulator that has been shown to be essential for the induction of systemic acquired resistance. In npr1 mutant plants, salicylic acid (SA)–mediated PR gene expression and pathogen resistance are abolished completely. NPR1 has been shown to interact with three closely related TGA transcription factors—TGA2, TGA5, and TGA6—in yeast two-hybrid assays. To elucidate the biological functions of these three TGA transcription factors, we analyzed single and combined deletion knockout mutants of TGA2, TGA5, and TGA6 for SA-induced PR gene expression and pathogen resistance. Induction of PR gene expression and pathogen resistance by the SA analog 2,6-dichloroisonicotinic acid (INA) was blocked in tga6-1 tga2-1 tga5-1 but not in tga6-1 or tga2-1 tga5-1 plants. Loss of INA-induced resistance to Peronospora parasitica Noco2 cosegregated with the tga6-1 mutation in progeny of multiple lines that were heterozygous for tga6-1 and homozygous for tga2-1 tga5-1 and could be complemented by genomic clones of wild-type TGA2 or TGA5, indicating that TGA2, TGA5, and TGA6 encode redundant and essential functions in the positive regulation of systemic acquired resistance. In addition, tga6-1 tga2-1 tga5-1 plants had reduced tolerance to high levels of SA and accumulated higher basal levels of PR-1 under noninducing conditions, suggesting that these TGA factors also are important for SA tolerance and the negative regulation of the basal expression of PR-1.
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