Abstract

Xanthomonas type III effector AvrBsT induces hypersensitive cell death and defence responses in pepper (Capsicum annuum) and Nicotiana benthamiana. Little is known about the host factors that interact with AvrBsT. Here, we identified pepper aldehyde dehydrogenase 1 (CaALDH1) as an AvrBsT-interacting protein. Bimolecular fluorescence complementation and co-immunoprecipitation assays confirmed the interaction between CaALDH1 and AvrBsT in planta. CaALDH1:smGFP fluorescence was detected in the cytoplasm. CaALDH1 expression in pepper was rapidly and strongly induced by avirulent Xanthomonas campestris pv. vesicatoria (Xcv) Ds1 (avrBsT) infection. Transient co-expression of CaALDH1 with avrBsT significantly enhanced avrBsT-triggered cell death in N. benthamiana leaves. Aldehyde dehydrogenase activity was higher in leaves transiently expressing CaALDH1, suggesting that CaALDH1 acts as a cell death enhancer, independently of AvrBsT. CaALDH1 silencing disrupted phenolic compound accumulation, H2O2 production, defence response gene expression, and cell death during avirulent Xcv Ds1 (avrBsT) infection. Transgenic Arabidopsis thaliana overexpressing CaALDH1 exhibited enhanced defence response to Pseudomonas syringae pv. tomato and Hyaloperonospora arabidopsidis infection. These results indicate that cytoplasmic CaALDH1 interacts with AvrBsT and promotes plant cell death and defence responses.

Highlights

  • Microbial pathogens attack plants to acquire nutrients for growth, development, and reproduction (Dangl et al, 2013)

  • Transgenic Arabidopsis thaliana overexpressing clone was designated pepper aldehyde dehydrogenase 1 (CaALDH1) exhibited enhanced defence response to Pseudomonas syringae pv. tomato and Hyaloperonospora arabidopsidis infection. These results indicate that cytoplasmic CaALDH1 interacts with AvrBsT and promotes plant cell death and defence responses

  • A prey library was generated by fusing the activation domain (AD) to pepper cDNAs synthesized from transcripts of pepper leaves undergoing hypersensitive response (HR), and AvrBsT was fused to the binding domain (BD) and used as bait to screen the library

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Summary

Introduction

Microbial pathogens attack plants to acquire nutrients for growth, development, and reproduction (Dangl et al, 2013). The first tier of the plant immune system contains pattern-recognition receptors (PRRs) localized on the cell surface that bind to evolutionarily conserved pathogenassociated molecular patterns (PAMPs) (Jones and Dangl, 2006; Dodds and Rathjen, 2010; Monaghan and Zipfel, 2012). PRRs bind to the pathogen-derived ligand, become 3368 | Kim and Hwang activated, and trigger an intracellular signalling cascade that drives transcriptional reprogramming and defence molecule biosynthesis to inhibit pathogen colonization (Monaghan and Zipfel, 2012). NLR proteins recognize specific pathogen effectors either via direct interaction with the effector protein (Dodds et al, 2006) or via recognition of pathogen effector-mediated modifications (van der Hoorn and Kamoun, 2008)

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