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Plant WRKY DNA-binding transcription factors are involved in plant responses to biotic …


Biology Articles » Botany » Plant Pathology » Roles of Arabidopsis WRKY3 and WRKY4 Transcription Factors in Plant Responses to Pathogens » Background

Background
- Roles of Arabidopsis WRKY3 and WRKY4 Transcription Factors in Plant Responses to Pathogens

Upon pathogen infection, pathogen-associated molecular patterns (PAMPs) such as bacterial flagellin and lipopolysaccharides are recognized by plant receptors to activate PAMP-triggered immunity through a mitogen-activated protein kinase signaling cascade [1]. Gram-negative bacterial pathogens such as Pseudomonas syringae can deliver effector proteins to plant cells to interfere PAMP-triggered resistance to promote pathogen virulence. As a result, the remaining basal defense is usually insufficient to contain pathogens but can limit their growth in plant tissue. Through co-evolution, some effectors may be specifically recognized by plant resistance (R) proteins and activate strong effector-triggered immunity (ETI) [1]. R gene-activated ETI involves a complex defense program including production of reactive oxygen species (ROS) and salicylic acid (SA), rapid programmed cell death (hypersensitive responses, HR) and induction of a large number of host genes including pathogenesis-related (PR) genes [1]. In Arabidopsis, R gene- and SA-mediated defense mechanisms are effective against biotrophic pathogens that feed on living host tissue during the whole or part of their infection cycle [2,3].

Necrotrophic pathogens kill the host to extract nutrients. Many necrotrophic pathogens produce toxins, cell wall-degrading enzymes and ROS to promote disease and macerate plant tissue [4]. Plant defense mechanisms against necrotrophic pathogens have been analyzed relatively recently and appear to differ from those against biotrophic pathogens in important ways. First, gene-for-gene resistance is common to biotrophic pathogens but not to necrotrophic pathogens. Second, R gene-mediated HR is effective against biotrophic pathogens but does not deter and in some cases actually facilitate infection of necrotrophic pathogens [5]. Third, while SA is important for resistance to biotrophic pathogens, its role in defense against necrotrophic pathogens is limited, if any. In Arabidopsis, mutations that impair SA biosynthesis or signaling do not affect resistance to Botrytis [6,7]. Abolishing SA accumulation in transgenic nahG plants resulted in limited increase in susceptibility to Botrytis [6]. However, transgenic nahG plants have nonspecific phenotypes (i.g. reduced phytoalexin) independent of SA [8,9] and the enhanced susceptibility to Botrytis observed in transgenic nahG plants may not be caused by SA deficiency.

Although discovered relatively recently, WRKY transcription factors are becoming one of the best-characterized classes of plant transcription factors and are at the forefront of research on plant defense responses [10]. Pathogen infection or treatment with pathogen elicitors or SA induces rapid expression of plant WRKY genes. We have shown that in Arabidopsis, for example, expression of 49 out of 72 tested WRKY genes was differentially regulated after pathogen infection or SA treatment [11]. In addition, a large number of defense or defense-related genes, including well-studied PR genes and the regulatory NPR1 gene, contain W-box elements in their promoters that are specifically recognized by WRKY proteins and are necessary for their inducible expression [12-18]. More recent studies have provided direct evidence for the involvement of specific WRKY proteins in plant defense responses. For example, mutations of Arabidopsis WRKY70 enhance plant susceptibility to both biotrophic and necrotrophic pathogens including the bacterial pathogen Erwinia carotovora as well as fungal pathogens Erysiphe cichoracearum and Botrytis [19-21]. In addition, wrky70 mutants are compromised in both basal and R-gene (RPP4)-mediated resistance to the oomycete Hyaloperonospora parasitica [22]. Arabidopsis wrky33 mutants are highly susceptible to necrotrophic pathogens but respond normally to biotrophic pathogens [23]. These results indicate that WRKY33 plays an important and specific role in plant resistance to necrotrophic pathogens. Other WRKY proteins can function as negative regulators of plant disease resistance. For example, mutations of Arabidopsis WRKY7, WRKY11 and WRKY17 enhance plant resistance to virulent P. syringae strains [24-26] and mutations of Arabidopsis WRKY25 enhance tolerance to P. syringae [27]. The structurally related WRKY18, WRKY40 and WRKY60 function partially redundantly as negative regulators in plant resistance to P. syringae and E. orontii [28,29]. Their barley homologues HvWRKY1 and HvWRKY2 also function as suppressors of basal defense [29]. The diverse roles of WRKY proteins may reflect the complex signaling and transcriptional networks of plant defense that require tight regulation and fine-tuning.

We have previously shown that infection of an avirulent P. syringae strain or SA treatment induces Arabidopsis WRKY3 and WRKY4, which encode two structurally closely related WRKY proteins [11]. In the present study, we have shown that both WRKY3 and WRKY4 are nuclear-localized sequence-specific DNA-binding proteins. We have also shown that induced expression of WRKY3 and WRKY4 after pathogen infection or SA treatment was primarily due to plant stress caused by infiltration and spraying of pathogen suspension or SA solution. Both loss-of-function T-DNA insertion mutants and transgenic overexpression lines for WRKY3 and WRKY4 have been generated and examined for responses to the biotrophic bacterial pathogen P. syringae and the necrotrophic fungal pathogen B. cinerea. These studies strongly suggested that WRKY3 and WRKY4 play a positive role in plant resistance to necrotrophic pathogens but a negative role in resistance to biotrophic pathogens.


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