Resistance to hemi-biotrophic F. graminearum infection is associated with coordinated and ordered expression of diverse defense signaling pathways.

Lina Ding,Shulin Xue,Zhengqiang Ma,Liming Yang,Haibin Xu,Haiyan Jia,Lixia Zhang,Zhongxin Kong,Hongying Yi,Miguel A Blazquez

doi:10.1371/journal.pone.0019008

Abstract

Fusarium species cause serious diseases in cereal staple food crops such as wheat and maize. Currently, the mechanisms underlying resistance to Fusarium-caused diseases are still largely unknown. In the present study, we employed a combined proteomic and transcriptomic approach to investigate wheat genes responding to F. graminearum infection that causes Fusarium head blight (FHB). We found a total of 163 genes and 37 proteins that were induced by infection. These genes and proteins were associated with signaling pathways mediated by salicylic acid (SA), jasmonic acid (JA), ethylene (ET), calcium ions, phosphatidic acid (PA), as well as with reactive oxygen species (ROS) production and scavenging, antimicrobial compound synthesis, detoxification, and cell wall fortification. We compared the time-course expression profiles between FHB-resistant Wangshuibai plants and susceptible Meh0106 mutant plants of a selected set of genes that are critical to the plants' resistance and defense reactions. A biphasic phenomenon was observed during the first 24 h after inoculation (hai) in the resistant plants. The SA and Ca2+ signaling pathways were activated within 6 hai followed by the JA mediated defense signaling activated around 12 hai. ET signaling was activated between these two phases. Genes for PA and ROS synthesis were induced during the SA and JA phases, respectively. The delayed activation of the SA defense pathway in the mutant was associated with its susceptibility. After F. graminearum infection, the endogenous contents of SA and JA in Wangshuibai and the mutant changed in a manner similar to the investigated genes corresponding to the individual pathways. A few genes for resistance-related cell modification and phytoalexin production were also identified. This study provided important clues for designing strategies to curb diseases caused by Fusarium.

Highlights

Plants have evolved multiple layers of passive and active defense mechanisms to combat microbial pathogen attack in order to maintain their growth or survival
The compromised resistance of Meh0106 to infection and the spread of F. graminearum within Meh0106 spikes were validated in repeated trials (Table 1)
We found that the gene for 1-aminocyclopropane-1-carboxylic acid oxidase (ACO) enzyme catalyzing the oxidation of ACC to ethylene, and the gene for jasmonate biosynthesis isoenzyme 12oxophytodienoate reductase 3 (12-OPR3) were both only elevated in Wangshuibai (Table S1)

Summary

Introduction

Plants have evolved multiple layers of passive and active defense mechanisms to combat microbial pathogen attack in order to maintain their growth or survival. Passive defense takes advantage of preexisting structures [1] and preformed antimicrobial or toxic secondary metabolites, proteins, or peptides [2]. Active defenses, such as oxidative burst induction [3], hypersensitive response (HR) [4], accumulation of toxic compounds [5], and fortification of cell walls [6], are triggered rapidly and directly in response to pathogen attack. Active plant defense is finely regulated to survive adversity at a minimum expense to growth This regulation is multifaceted and might vary depending on the plant taxa and the pathogen lifestyle. The innate plant immunity system known as pathogen-associated molecular patterns (PAMP), or PAMP-triggered immunity (PTI)

Methods

Results

Conclusion