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Gene Review

AHBP-1B  -  transcription factor TGA2

Arabidopsis thaliana

Synonyms: MOJ9.12, MOJ9_12, TGA2, TGACG sequence-specific binding protein 2
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High impact information on AHBP-1B

  • We show that TGA2 and NPR1 are recruited to PR-1 independently of each other and of SA treatment [1].
  • 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 [2].
  • Because leaf transfection assays indicate that TGA3 activates transcription, as noted previously for TGA2, these two TGA factors are predicted to make positive contributions to the expression of this target gene [3].
  • Knockout analysis of Arabidopsis transcription factors TGA2, TGA5, and TGA6 reveals their redundant and essential roles in systemic acquired resistance [2].
  • These genetic data clearly demonstrate that TGA2 is a SA-responsive and NPR1-dependent transcription activator [4].

Biological context of AHBP-1B


Anatomical context of AHBP-1B


Associations of AHBP-1B with chemical compounds

  • Protein-DNA complexes resulting from the formaldehyde fixation of leaves of plants 2 h after exposure to 1 mm salicylic acid (SA) were immunoprecipitated using antibodies against the TGA2 transcription factor [6].

Physical interactions of AHBP-1B

  • Coupled with observations that the DNA binding activity of TGA factors is deregulated in npr1 plants, the results suggest that NPR1-mediated DNA binding of TGA2 is critical for activation of defense genes [8].

Other interactions of AHBP-1B


Analytical, diagnostic and therapeutic context of AHBP-1B

  • Genomic Southern blot analysis confirmed that TGA2 is a member of the gene family [9].
  • Furthermore, a gel mobility shift assay showed that the purified transcription factor protein, AHBP-1b, binds specifically to an SA-responsive promoter element of the A. thaliana PR-1 gene [10].


  1. The Coactivator Function of Arabidopsis NPR1 Requires the Core of Its BTB/POZ Domain and the Oxidation of C-Terminal Cysteines. Rochon, A., Boyle, P., Wignes, T., Fobert, P.R., Després, C. Plant Cell (2006) [Pubmed]
  2. Knockout analysis of Arabidopsis transcription factors TGA2, TGA5, and TGA6 reveals their redundant and essential roles in systemic acquired resistance. Zhang, Y., Tessaro, M.J., Lassner, M., Li, X. Plant Cell (2003) [Pubmed]
  3. Salicylic acid and NPR1 induce the recruitment of trans-activating TGA factors to a defense gene promoter in Arabidopsis. Johnson, C., Boden, E., Arias, J. Plant Cell (2003) [Pubmed]
  4. In vivo interaction between NPR1 and transcription factor TGA2 leads to salicylic acid-mediated gene activation in Arabidopsis. Fan, W., Dong, X. Plant Cell (2002) [Pubmed]
  5. TGA3 is a distinct member of the TGA family of bZIP transcription factors in Arabidopsis thaliana. Miao, Z.H., Liu, X., Lam, E. Plant Mol. Biol. (1994) [Pubmed]
  6. Development of Arabidopsis whole-genome microarrays and their application to the discovery of binding sites for the TGA2 transcription factor in salicylic acid-treated plants. Thibaud-Nissen, F., Wu, H., Richmond, T., Redman, J.C., Johnson, C., Green, R., Arias, J., Town, C.D. Plant J. (2006) [Pubmed]
  7. Negative regulation of defense responses in Arabidopsis by two NPR1 paralogs. Zhang, Y., Cheng, Y.T., Qu, N., Zhao, Q., Bi, D., Li, X. Plant J. (2006) [Pubmed]
  8. The Arabidopsis NPR1/NIM1 protein enhances the DNA binding activity of a subgroup of the TGA family of bZIP transcription factors. Després, C., DeLong, C., Glaze, S., Liu, E., Fobert, P.R. Plant Cell (2000) [Pubmed]
  9. Binding specificity and tissue-specific expression pattern of the Arabidopsis bZIP transcription factor TGA2. de Pater, S., Pham, K., Memelink, J., Kijne, J. Mol. Gen. Genet. (1996) [Pubmed]
  10. Interaction of NPR1 with basic leucine zipper protein transcription factors that bind sequences required for salicylic acid induction of the PR-1 gene. Zhang, Y., Fan, W., Kinkema, M., Li, X., Dong, X. Proc. Natl. Acad. Sci. U.S.A. (1999) [Pubmed]
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