Arabidopsis AtERF15 positively regulates immunity against Pseudomonas syringae pv. tomato DC3000 and Botrytis cinerea

Huijuan Zhang

doi:10.3389/fpls.2015.00686

Abstract

Upon pathogen infection, activation of immune response requires effective transcriptional reprogramming that regulates inducible expression of a large set of defense genes. A number of ethylene-responsive factor transcription factors have been shown to play critical roles in regulating immune responses in plants. In the present study, we explored the functions of Arabidopsis AtERF15 in immune responses against Pseudomonas syringae pv. tomato (Pst) DC3000, a (hemi)biotrophic bacterial pathogen, and Botrytis cinerea, a necrotrophic fungal pathogen. Expression of AtERF15 was induced by infection of Pst DC3000 and B. cinerea and by treatments with salicylic acid (SA) and methyl jasmonate. Biochemical assays demonstrated that AtERF15 is a nucleus-localized transcription activator. The AtERF15-overexpressing (AtERF15-OE) plants displayed enhanced resistance while the AtERF15-RNAi plants exhibited decreased resistance against Pst DC3000 and B. cinerea. Meanwhile, Pst DC3000- or B. cinerea-induced expression of defense genes was upregulated in AtERF15-OE plants but downregulated in AtERF15-RNAi plants, as compared to the expression in wild type plants. In response to infection with B. cinerea, the AtERF15-OE plants accumulated less reactive oxygen species (ROS) while the AtERF15-RNAi plants accumulated more ROS. The flg22- and chitin-induced oxidative burst was abolished and expression levels of the pattern-triggered immunity-responsive genes AtFRK1 and AtWRKY53 were suppressed in AtER15-RNAi plants upon treatment with flg22 or chitin. Furthermore, SA-induced defense response was also partially impaired in the AtERF15-RNAi plants. These data demonstrate that AtERF15 is a positive regulator of multiple layers of the immune responses in Arabidopsis.

Highlights

Plants have evolved to possess a sophisticated innate immune system to defend themselves against pathogen attack during their lifespan (Boller and He, 2009; Dodds and Rathjen, 2010; Schwessinger and Ronald, 2012; Fu and Dong, 2013)
RNAi-mediated suppression of AtERF15 attenuated flg22- and chitininduced PTI response (Figure 7) and partially impaired the SAinduced defense response (Figure 8). These findings demonstrate that AtERF15 acts as a positive regulator of Arabidopsis immune responses against Pst DC3000 and B. cinerea, representing a hemibiotrophic bacterial pathogen and a necrotrophic fungal pathogen, respectively
Defense responses againstbiotrophic pathogens such as Pst DC3000 are modulated via the salicylic acid (SA) signaling pathway, while defense responses against necrotrophic pathogens like B. cinerea are thought to be mediated by the JA/ET signaling pathways (Glazebrook, 2005; Grant and Jones, 2009; Verhage et al, 2010)

Summary

Introduction

Plants have evolved to possess a sophisticated innate immune system to defend themselves against pathogen attack during their lifespan (Boller and He, 2009; Dodds and Rathjen, 2010; Schwessinger and Ronald, 2012; Fu and Dong, 2013). Two types of innate immune responses that are timely activated and precisely regulated by different types of pathogens have been recognized in. In addition to the innate immunity, plants have developed to possess several forms of inducible immunity that becomes activated upon pathogen infection or treatment of elicitors. Once the pathogenderived PAMPs or effectors and elicitors are perceived (Boller and He, 2009), a battery of immune responses is often activated by a network of defense hormone-mediated signaling pathways (Pieterse et al, 2009), which lead to transcriptional reprogramming that coordinately regulates expression of a large set of genes. TFs are divided into diverse families according to conserved structural domains, which are involved in DNA binding activity and numerous TFs belonging to the AP2/ERF, NAC, WRKY, and bZIP families have been implicated in plant immune responses against diverse pathogens (Gutterson and Reuber, 2004; Alves et al, 2013; Nuruzzaman et al, 2013; Seo et al, 2015)

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Conclusion