NPR1 enhances the DNA binding activity of the Arabidopsis bZIP transcription factor TGA7

被引:21
作者
Shearer, Heather L. [1 ]
Wang, Lipu [2 ]
DeLong, Catherine [1 ]
Despres, Charles [3 ]
Fobert, Pierre R. [1 ]
机构
[1] Natl Res Council Canada, Inst Plant Biotechnol, Saskatoon, SK S7N 0W9, Canada
[2] Univ Saskatchewan, Dept Biol, Saskatoon, SK S7N 5E2, Canada
[3] Brock Univ, Dept Biol Sci, St Catharines, ON L2S 3A1, Canada
关键词
plant defense response; transcription; pathogenesis-related genes; salicylic acid; protein-protein interaction; SYSTEMIC ACQUIRED-RESISTANCE; SALICYLIC-ACID; DISEASE RESISTANCE; PR-1; GENE; EXPRESSION PATTERN; PROTEIN; THALIANA; FAMILY; ACTIVATION; INDUCTION;
D O I
10.1139/B08-143
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
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.
引用
收藏
页码:561 / 570
页数:10
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