51. NPR1 enhances the DNA binding activity of theArabidopsisbZIP transcription factor TGA7This paper is one of a selection of papers published in a Special Issue from the National Research Council of Canada – Plant Biotechnology Institute
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Pierre R. FobertP.R. Fobert, Heather L. ShearerH.L. Shearer, Lipu WangL. Wang, Charles Després, and Catherine DeLongC. DeLong
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Genetics ,Ecology ,fungi ,Response element ,Promoter ,Plant Science ,Biology ,biology.organism_classification ,Genome ,Transcription (biology) ,Arabidopsis ,Transcription factor ,Reprogramming ,Gene ,Ecology, Evolution, Behavior and Systematics - Abstract
Pathogen-induced transcriptional reprogramming of the plant genome is mediated predominantly by the cofactor NPR1 (NON-EXPRESSOR OF PATHOGENESIS-RELATED GENES1). NPR1 lacks any known DNA-binding domain and is proposed to regulate transcription through interactions with TGA transcription factors that bind to as-1-like promoter elements. Previous studies have focused on the interaction of NPR1 with subgroup I (TGA1, TGA4) or subgroup II (TGA2, TGA5, TGA6) factors. Using the yeast two-hybrid system, we showed that a member of subgroup III (TGA7) interacts with wild-type NPR1 but not with mutants in the ankyrin repeats that are important for disease resistance. Mutations in the NPR1 BTB/POZ domain also greatly reduced interaction with TGA7. NPR1 substantially increased the binding of TGA7 to cognate promoter elements in vitro, including a salicylic-acid-inducible element of the PR-1 promoter. While TGA7 interacted with all TGA factors tested, interactions were not observed between TGA2 and subgroup I factors, indicating that cross-clade interaction is not a general property of the family. Transcripts from subgroup III TGA factors were weakly inducible by salicylic acid and pathogens, but only TGA3 expression was dependent on NPR1. These results suggest that NPR1-mediated DNA binding of TGA7 could regulate the activation of defense genes.
- Published
- 2009
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