Literature DB >> 11161032

A comparison of the effects of DNA-damaging agents and biotic elicitors on the induction of plant defense genes, nuclear distortion, and cell death.

J J Choi1, S J Klosterman, L A Hadwiger.   

Abstract

Pea (Pisum sativum L. cv Alcan) endocarp tissue challenged with an incompatible fungal pathogen, Fusarium solani f. sp. phaseoli or fungal elicitors results in the induction of pathogenesis-related (PR) genes and the accumulation of pisatin, a phytoalexin. Essentially the same response occurs in pea tissue exposed to DNA-specific agents that crosslink or intercalate DNA. In this study, the effects of DNA-damaging agents were assessed relative to the inducible expression of several pea PR genes: phenylalanine ammonia lyase, chalcone synthase, and DRR206. Mitomycin C and actinomycin D mimicked the biotic elicitors in enhancing the expression of all three PR genes. The activities of these PR gene promoters, isolated from different plants, were evaluated heterologously in transgenic tobacco. It is remarkable that beta-glucuronidase expression was induced when plants containing the heterologous phenylalanine ammonia lyase, chalcone synthase, and DRR206 promoter-beta-glucuronidase chimeric reporter genes were treated by DNA-damaging agents. Finally, cytological analyses indicated that many of these agents caused nuclear distortion and collapse of the treated pea cells. Yet we observed that cell death is not necessary for the induction of the PR gene promoters assessed in this study. Based on these observations and previously published results, we propose that DNA damage or the associated alteration of chromatin can signal the transcriptional activation of plant defense genes.

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Year:  2001        PMID: 11161032      PMCID: PMC64876          DOI: 10.1104/pp.125.2.752

Source DB:  PubMed          Journal:  Plant Physiol        ISSN: 0032-0889            Impact factor:   8.340


  42 in total

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Review 4.  Anatomy of a nonhost disease resistance response of pea to Fusarium solani: PR gene elicitation via DNase, chitosan and chromatin alterations.

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