NPR1 differentially interacts with members of the TGA/OBF family of transcription factors that bind an element of the PR-1 gene required for induction by salicylic acid.

NPR1 is a critical component of the salicylic acid (SA)-mediated signal transduction pathway leading to the induction of defense genes, such as the pathogenesis-related (PR)-1 gene, and enhanced disease resistance. Using a yeast two-hybrid screen, we identified several NPR1-interacting proteins (NIPs). Two of these NIPs are members of the TGA/OBF family of basic leucine zipper (bZIP) transcription factors; this family has been implicated in the activation of SA-responsive genes, including PR-1. Six TGA family members were tested and shown to differentially interact with NPR1: TGA2 and TGA3 showed strong affinity for NPR1; TGA5 and TGA6 exhibited weaker affinity; and TGA1 and TGA4 displayed little or no detectable interaction with NPR1, respectively. Interestingly, the amino-termini of these factors were found to decrease their stability in yeast and differentially affect their apparent affinity toward NPR1. The interacting regions on NPR1 and the TGA factors were also defined. Each of four point mutations in NPR1 that disrupt SA signaling in Arabidopsis completely blocked interaction of NPR1 with TGA2 and TGA3. TGA2 and TGA3 were also found to bind the SA-responsive element of the Arabidopsis PR-1 promoter. These results directly link NPR1 to SA-induced PR-1 expression through members of the TGA family of transcription factors.

[1]  S. Masters,et al.  14-3-3 proteins: structure, function, and regulation. , 2000, Annual review of pharmacology and toxicology.

[2]  D F Klessig,et al.  Characterization of a new Arabidopsis mutant exhibiting enhanced disease resistance. , 1999, Molecular plant-microbe interactions : MPMI.

[3]  Jyoti Shah,et al.  Salicylic acid and disease resistance in plants. , 1999 .

[4]  Xin Li,et al.  Interaction of NPR1 with basic leucine zipper protein transcription factors that bind sequences required for salicylic acid induction of the PR-1 gene. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

[5]  D. Klessig,et al.  The Arabidopsis ssi1 Mutation Restores Pathogenesis-Related Gene Expression in npr1 Plants and Renders Defensin Gene Expression Salicylic Acid Dependent , 1999, Plant Cell.

[6]  P. Heifetz,et al.  Functional analysis of regulatory sequences controlling PR-1 gene expression in Arabidopsis. , 1998, The Plant journal : for cell and molecular biology.

[7]  C. Pieterse,et al.  A Novel Signaling Pathway Controlling Induced Systemic Resistance in Arabidopsis , 1998, Plant Cell.

[8]  A. Bent,et al.  Gene-for-gene disease resistance without the hypersensitive response in Arabidopsis dnd1 mutant. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[9]  Xin Li,et al.  Generation of broad-spectrum disease resistance by overexpression of an essential regulatory gene in systemic acquired resistance. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[10]  D. Klessig,et al.  Uncoupling PR Gene Expression from NPR1 and Bacterial Resistance: Characterization of the Dominant Arabidopsis cpr6-1 Mutant , 1998, Plant Cell.

[11]  C. Stange,et al.  Phosphorylation of nuclear proteins directs binding to salicylic acid-responsive elements. , 1997, The Plant journal : for cell and molecular biology.

[12]  D F Klessig,et al.  The cpr5 mutant of Arabidopsis expresses both NPR1-dependent and NPR1-independent resistance. , 1997, The Plant cell.

[13]  W. Crosby,et al.  A plant cyclin-dependent kinase inhibitor gene , 1997, Nature.

[14]  A. Israël,et al.  IκB proteins: structure, function and regulation , 1997 .

[15]  J. Ryals,et al.  The Arabidopsis NIM1 protein shows homology to the mammalian transcription factor inhibitor I kappa B. , 1997, The Plant cell.

[16]  Jane Glazebrook,et al.  The Arabidopsis NPR1 Gene That Controls Systemic Acquired Resistance Encodes a Novel Protein Containing Ankyrin Repeats , 1997, Cell.

[17]  E. Lam,et al.  Switching of gene expression: analysis of the factors that spatially and temporally regulate plant gene expression. , 1997, Genetic engineering.

[18]  D. Klessig,et al.  Characterization of a salicylic acid-insensitive mutant (sai1) of Arabidopsis thaliana, identified in a selective screen utilizing the SA-inducible expression of the tms2 gene. , 1997, Molecular plant-microbe interactions : MPMI.

[19]  G. Chao,et al.  The promoter of a H2O2-inducible, Arabidopsis glutathione S-transferase gene contains closely linked OBF- and OBP1-binding sites. , 1996, The Plant journal : for cell and molecular biology.

[20]  C. Scheidereit,et al.  Different mechanisms control signal‐induced degradation and basal turnover of the NF‐kappaB inhibitor IkappaB alpha in vivo. , 1996, The EMBO journal.

[21]  E. Craig,et al.  Genomic libraries and a host strain designed for highly efficient two-hybrid selection in yeast. , 1996, Genetics.

[22]  N. Pavletich,et al.  Structure of the p53 Tumor Suppressor Bound to the Ankyrin and SH3 Domains of 53BP2 , 1996, Science.

[23]  David Baltimore,et al.  NF-κB: Ten Years After , 1996, Cell.

[24]  J. Ryals,et al.  Systemic Acquired Resistance. , 1996, The Plant cell.

[25]  N. Chua,et al.  Activation of the CaMV as‐1 cis‐element by salicylic acid: differential DNA‐binding of a factor related to TGA1a. , 1996, The EMBO journal.

[26]  R. Dixon,et al.  Tobacco plants epigenetically suppressed in phenylalanine ammonia‐lyase expression do not develop systemic acquired resistance in response to infection by tobacco mosaic virus , 1996 .

[27]  F. Ausubel,et al.  Isolation of Arabidopsis mutants with enhanced disease susceptibility by direct screening. , 1996, Genetics.

[28]  B. Mauch-Mani,et al.  Production of Salicylic Acid Precursors Is a Major Function of Phenylalanine Ammonia-Lyase in the Resistance of Arabidopsis to Peronospora parasitica. , 1996, The Plant cell.

[29]  J. Ryals,et al.  Suppression and Restoration of Lesion Formation in Arabidopsis lsd Mutants. , 1995, The Plant cell.

[30]  J. Ryals,et al.  Arabidopsis signal transduction mutant defective in chemically and biologically induced disease resistance. , 1995, Proceedings of the National Academy of Sciences of the United States of America.

[31]  G. Hagen,et al.  The Soybean GH2/4 Gene That Encodes a Glutathione S-Transferase Has a Promoter That Is Activated by a Wide Range of Chemical Agents , 1995, Plant physiology.

[32]  A. Willems,et al.  Studies on the transformation of intact yeast cells by the LiAc/SS‐DNA/PEG procedure , 1995, Yeast.

[33]  D. Klessig,et al.  A mutation in Arabidopsis that leads to constitutive expression of systemic acquired resistance. , 1994, The Plant cell.

[34]  E. Ward,et al.  A Central Role of Salicylic Acid in Plant Disease Resistance , 1994, Science.

[35]  Xinnian Dong,et al.  Characterization of an Arabidopsis Mutant That Is Nonresponsive to Inducers of Systemic Acquired Resistance. , 1994, The Plant cell.

[36]  J. Dangl,et al.  Arabidopsis mutants simulating disease resistance response , 1994, Cell.

[37]  F. Ausubel,et al.  Programmed cell death in plants: A pathogen-triggered response activated coordinately with multiple defense functions , 1994, Cell.

[38]  R. Foley,et al.  Isolation and characterization of two related Arabidopsis ocs-element bZIP binding proteins. , 1993, The Plant journal : for cell and molecular biology.

[39]  Leslie Friedrich,et al.  Requirement of Salicylic Acid for the Induction of Systemic Acquired Resistance , 1993, Science.

[40]  D. Klessig,et al.  Salicylic acid and plant disease resistance , 1992 .

[41]  E. Lam,et al.  A tobacco DNA binding protein that interacts with a light-responsive box II element. , 1992, The Plant cell.

[42]  F. Katagiri,et al.  Two tobacco DNA-binding proteins with homology to the nuclear factor CREB , 1989, Nature.

[43]  S. Fields,et al.  A novel genetic system to detect protein–protein interactions , 1989, Nature.

[44]  S. Ho,et al.  Site-directed mutagenesis by overlap extension using the polymerase chain reaction. , 1989, Gene.