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Gene Review

PDF1.2  -  ethylene- and jasmonate-responsive plant...

Arabidopsis thaliana

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Disease relevance of PDF1.2

  • Ectopic overproduction of GhHb1 in Arabidopsis led to constitutive expression of the defense genes PR-1 and PDF1.2, and conferred enhanced disease resistance to Pseudomonas syringae and tolerance to V. dahliae [1].
  • No transcripts for pathogenesis-related PR-1, PR-5, or the pathogen-inducible plant defensin Pdf1.2 could be detected in uninoculated transgenic seedlings, indicating that all of the observed effects of the overexpressing lines are most likely the result of the toxicity of the THI2.1 thionin [2].

High impact information on PDF1.2

  • Activation of the PDF1.2 and b-CHI, ethylene/JA-responsive genes, is, however, increased in these mutants [3].
  • By contrast, ssi2 plants are compromised in the induction of the jasmonic acid (JA)-responsive gene PDF1.2 and in resistance to the necrotrophic pathogen Botrytis cinerea [4].
  • Arabidopsis plants unable to accumulate SA produced 25-fold higher levels of JA and showed enhanced expression of the JA-responsive genes LOX2, PDF1.2, and VSP in response to infection by Pseudomonas syringae pv tomato DC3000, indicating that in wild-type plants, pathogen-induced SA accumulation is associated with the suppression of JA signaling [5].
  • Exogenous application of salicylic acid to Arabidopsis-Pti4 plants suppressed the increased expression of PDF1.2 but further stimulated PR1 expression [6].
  • Furthermore, exogenous application of BTH restored PDF1.2 expression in these plants [7].

Biological context of PDF1.2

  • Whereas the NADPH oxidase mutants were affected in UV-B-dependent CHS, PYROA and MEB5.2 gene expression, the mkp1 mutant was affected in the general expression pattern of the pathogenesis-related (PR) and PDF1.2 genes [8].
  • The observed up-regulation of the PDF1.2 gene in mutants defective in the SA-dependent signaling pathway points to a cross-talk between SA- and jasmonate/ethylene-dependent signaling pathways during pathogen ingress [9].
  • Using stably transformed plants, we first characterized the extended promoter region that positively regulates basal expression from the PDF1.2 promoter [10].
  • By analyzing the progeny of crosses between cpr22 plants and either NahG transgenic plants or npr1 mutants, all of the cpr22-associated phenotypes except PDF1.2 expression were found to be SA dependent [11].
  • While the induction of the AtEBP transgene and PDF1.2 had similar DEX concentration requirements, the kinetics of induction differed significantly, with the AtEBP transgene being induced within 1 h and PDF1.2 only being induced between 24 and 48 h [12].

Associations of PDF1.2 with chemical compounds

  • Here, we report the isolation and characterization of a 23-aa peptide from Arabidopsis, called AtPep1, which activates transcription of the defensive gene defensin (PDF1.2) and activates the synthesis of H(2)O(2), both being components of the innate immune response [13].
  • In the present study, we show that, in addition to SA, ethylene and JA signaling also are required for the ssi1-conferred constitutive expression of PDF1.2 and the NPR1-independent expression of PR-1 [14].
  • In support of this idea, we observed a marked synergy between ethylene and methyl jasmonate for the induction of PDF1.2 in plants grown under sterile conditions [15].
  • These suggested that there was a transient synergistic enhancement in the expression of genes associated with either JA (PDF1.2 [defensin] and Thi1.2 [thionin]) or SA (PR1 [PR1a-beta-glucuronidase in tobacco]) signaling when both signals were applied at low (typically 10-100 microm) concentrations [16].
  • PDF1.2, a plant defensin gene, was strongly induced in all transgenic lines examined following treatment with DEX, including empty vector lines that did not show any observable DEX-induced growth defect [12].

Regulatory relationships of PDF1.2


Other interactions of PDF1.2

  • Ectopic CAPIP2 expression in Arabidopsis was accompanied by the expression of Arabidopsis PR-1 and PDF1.2 genes [18].
  • However, the cpr5 npr1 plants retained heightened resistance to P. parasitica Noco2 and elevated expression of the defensin gene PDF1.2, implying that NPR1-independent resistance signaling also occurs [19].
  • A large number of well-known JA responsive genes showed the same expression profile, including genes involved in storage of amino acids (VSP), glucosinolate production (CYP79), polyamine biosynthesis (ADC2), and defense (PDF1.2) [20].
  • Analysis of the expression profiles of PR-1, BGL2, PR-5 and PDF1.2 in eds14, eds15, and eds16 revealed differences from the wild type for all the lines [21].
  • The Arabidopsis vegetative storage protein (AtVSP) and plant defense-related proteins thionin (Thi2.1) and defensin (PDF1.2) have previously been shown to accumulate in response to JA induction [22].

Analytical, diagnostic and therapeutic context of PDF1.2


  1. Ectopic Expression of the Cotton Non-symbiotic Hemoglobin Gene GhHbd1 Triggers Defense Responses and Increases Disease Tolerance in Arabidopsis. Qu, Z.L., Zhong, N.Q., Wang, H.Y., Chen, A.P., Jian, G.L., Xia, G.X. Plant Cell Physiol. (2006) [Pubmed]
  2. Overexpression of an endogenous thionin enhances resistance of Arabidopsis against Fusarium oxysporum. Epple, P., Apel, K., Bohlmann, H. Plant Cell (1997) [Pubmed]
  3. Conserved MYC transcription factors play a key role in jasmonate signaling both in tomato and Arabidopsis. Boter, M., Ruíz-Rivero, O., Abdeen, A., Prat, S. Genes Dev. (2004) [Pubmed]
  4. Plastidial fatty acid signaling modulates salicylic acid- and jasmonic acid-mediated defense pathways in the Arabidopsis ssi2 mutant. Kachroo, A., Lapchyk, L., Fukushige, H., Hildebrand, D., Klessig, D., Kachroo, P. Plant Cell (2003) [Pubmed]
  5. NPR1 modulates cross-talk between salicylate- and jasmonate-dependent defense pathways through a novel function in the cytosol. Spoel, S.H., Koornneef, A., Claessens, S.M., Korzelius, J.P., Van Pelt, J.A., Mueller, M.J., Buchala, A.J., Métraux, J.P., Brown, R., Kazan, K., Van Loon, L.C., Dong, X., Pieterse, C.M. Plant Cell (2003) [Pubmed]
  6. Tomato transcription factors pti4, pti5, and pti6 activate defense responses when expressed in Arabidopsis. Gu, Y.Q., Wildermuth, M.C., Chakravarthy, S., Loh, Y.T., Yang, C., He, X., Han, Y., Martin, G.B. Plant Cell (2002) [Pubmed]
  7. The Arabidopsis ssi1 mutation restores pathogenesis-related gene expression in npr1 plants and renders defensin gene expression salicylic acid dependent. Shah, J., Kachroo, P., Klessig, D.F. Plant Cell (1999) [Pubmed]
  8. The role of NADPH oxidase and MAP kinase phosphatase in UV-B-dependent gene expression in Arabidopsis. Kalbina, I., Strid, A. Plant Cell Environ. (2006) [Pubmed]
  9. beta-Aminobutyric acid-induced protection of Arabidopsis against the necrotrophic fungus Botrytis cinerea. Zimmerli, L., Métraux, J.P., Mauch-Mani, B. Plant Physiol. (2001) [Pubmed]
  10. A role for the GCC-box in jasmonate-mediated activation of the PDF1.2 gene of Arabidopsis. Brown, R.L., Kazan, K., McGrath, K.C., Maclean, D.J., Manners, J.M. Plant Physiol. (2003) [Pubmed]
  11. Environmentally sensitive, SA-dependent defense responses in the cpr22 mutant of Arabidopsis. Yoshioka, K., Kachroo, P., Tsui, F., Sharma, S.B., Shah, J., Klessig, D.F. Plant J. (2001) [Pubmed]
  12. A glucocorticoid-inducible transcription system causes severe growth defects in Arabidopsis and induces defense-related genes. Kang, H.G., Fang, Y., Singh, K.B. Plant J. (1999) [Pubmed]
  13. An endogenous peptide signal in Arabidopsis activates components of the innate immune response. Huffaker, A., Pearce, G., Ryan, C.A. Proc. Natl. Acad. Sci. U.S.A. (2006) [Pubmed]
  14. Ethylene and jasmonic acid signaling affect the NPR1-independent expression of defense genes without impacting resistance to Pseudomonas syringae and Peronospora parasitica in the Arabidopsis ssi1 mutant. Nandi, A., Kachroo, P., Fukushige, H., Hildebrand, D.F., Klessig, D.F., Shah, J. Mol. Plant Microbe Interact. (2003) [Pubmed]
  15. Concomitant activation of jasmonate and ethylene response pathways is required for induction of a plant defensin gene in Arabidopsis. Penninckx, I.A., Thomma, B.P., Buchala, A., Métraux, J.P., Broekaert, W.F. Plant Cell (1998) [Pubmed]
  16. The outcomes of concentration-specific interactions between salicylate and jasmonate signaling include synergy, antagonism, and oxidative stress leading to cell death. Mur, L.A., Kenton, P., Atzorn, R., Miersch, O., Wasternack, C. Plant Physiol. (2006) [Pubmed]
  17. Arabidopsis WRKY33 transcription factor is required for resistance to necrotrophic fungal pathogens. Zheng, Z., Qamar, S.A., Chen, Z., Mengiste, T. Plant J. (2006) [Pubmed]
  18. Identification and functional expression of the pepper pathogen-induced gene, CAPIP2, involved in disease resistance and drought and salt stress tolerance. Lee, S.C., Kim, S.H., An, S.H., Yi, S.Y., Hwang, B.K. Plant Mol. Biol. (2006) [Pubmed]
  19. The cpr5 mutant of Arabidopsis expresses both NPR1-dependent and NPR1-independent resistance. Bowling, S.A., Clarke, J.D., Liu, Y., Klessig, D.F., Dong, X. Plant Cell (1997) [Pubmed]
  20. The potassium-dependent transcriptome of Arabidopsis reveals a prominent role of jasmonic acid in nutrient signaling. Armengaud, P., Breitling, R., Amtmann, A. Plant Physiol. (2004) [Pubmed]
  21. Three unique mutants of Arabidopsis identify eds loci required for limiting growth of a biotrophic fungal pathogen. Dewdney, J., Reuber, T.L., Wildermuth, M.C., Devoto, A., Cui, J., Stutius, L.M., Drummond, E.P., Ausubel, F.M. Plant J. (2000) [Pubmed]
  22. An Arabidopsis mutant cex1 exhibits constant accumulation of jasmonate-regulated AtVSP, Thi2.1 and PDF1.2. Xu, L., Liu, F., Wang, Z., Peng, W., Huang, R., Huang, D., Xie, D. FEBS Lett. (2001) [Pubmed]
  23. The promoter of the plant defensin gene PDF1.2 from Arabidopsis is systemically activated by fungal pathogens and responds to methyl jasmonate but not to salicylic acid. Manners, J.M., Penninckx, I.A., Vermaere, K., Kazan, K., Brown, R.L., Morgan, A., Maclean, D.J., Curtis, M.D., Cammue, B.P., Broekaert, W.F. Plant Mol. Biol. (1998) [Pubmed]
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