The Arabidopsis defensin gene, AtPDF1.1, mediates defence against Pectobacterium carotovorum subsp. carotovorum via an iron-withholding defence system

Pao-Yuan Hsiao,Kah Wee Koh,Ming-Tsair Chan,Chiu-Ping Cheng

doi:10.1038/s41598-017-08497-7

Abstract

Plant defensins (PDFs) are cysteine-rich peptides that have a range of biological functions, including defence against fungal pathogens. However, little is known about their role in defence against bacteria. In this study, we showed that the protein encoded by ARABIDOPSIS THALIANA PLANT DEFENSIN TYPE 1.1 (AtPDF1.1) is a secreted protein that can chelate apoplastic iron. Transcripts of AtPDF1.1 were induced in both systemic non-infected leaves of Arabidopsis thaliana plants and those infected with the necrotrophic bacterium Pectobacterium carotovorum subsp. carotovorum (Pcc). The expression levels of AtPDF1.1 with correct subcellular localization in transgenic A. thaliana plants were positively correlated with tolerance to Pcc, suggesting its involvement in the defence against this bacterium. Expression analysis of genes associated with iron homeostasis/deficiency and hormone signalling indicated that the increased sequestration of iron by apoplastic AtPDF1.1 overexpression perturbs iron homeostasis in leaves and consequently activates an iron-deficiency-mediated response in roots via the ethylene signalling pathway. This in turn triggers ethylene-mediated signalling in systemic leaves, which is involved in suppressing the infection of necrotrophic pathogens. These findings provide new insight into the key functions of plant defensins in limiting the infection by the necrotrophic bacterium Pcc via an iron-deficiency-mediated defence response.

Highlights

Organisms have evolved multiple defence strategies for protection against pathogen attack, many of which are triggered by environmental cues
The results showed that the expression of AtPDF1.2a and AtPDF1.3, but not AtPDF1.1, was upregulated by ZnSO4 treatment (Fig. S1A), whereas transcript levels of these three AtPDF1 genes were upregulated by treatment with other essential divalent ions, such as FeSO4 and CuSO4 (Fig. S1B,C)
Since iron deficiency response occurred in the leaves and roots of AtPDF1.1 OE plants (Figs 4 and S10), we evaluated whether the state of iron deficiency induced by AtPDF1.1 overexpression led to activation of ethylene signalling in the roots

Summary

Introduction

Organisms have evolved multiple defence strategies for protection against pathogen attack, many of which are triggered by environmental cues One such strategy is the innate immune response, which utilizes Toll-like or pattern-recognition receptors to perceive specific pathogen-associated molecular patterns (PAMPs) that are derived from pathogens to trigger the defence signalling pathways. In plants, this process involves the activation of the salicylic acid (SA), jasmonic acid (JA) and ethylene (ET) signaling[1] pathways and the biosynthesis of defence molecules, such as antimicrobial peptides (AMPs)[2, 3], which cause membrane disruption, pore formation, and lead to cell lysis and death[4]. Fe-deficiency-induced transcription factor 1 (FIT1) has been shown to interact with other iron homeostasis responsive transcription factors, such as basic helix-loop-helix 38 and 39 (bHLH38 and bHLH 39), to activate the expression of FERRIC CHELATE REDUCTION OXIDASE 2 (FRO2) and IRON-REGULATED TRANSPORTER 1 (IRT1) in A. thaliana[20]

Methods

Results

Conclusion