Exploring the genetics of lesion and nodal resistance in pea (Pisum sativum L.) to Sclerotinia sclerotiorum using genome-wide association studies and RNA-Seq.

Hao‐Xun Chang,Xiaofeng Zhuang,Jie Wang,Hyunkyu Sang,Kevin E Mcphee,Martin I Chilvers,Lyndon D Porter

doi:10.1002/pld3.64

Hao‐Xun Chang, Xiaofeng Zhuang + Show 5 more

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https://doi.org/10.1002/pld3.64

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Abstract

The disease white mold caused by the fungus Sclerotinia sclerotiorum is a significant threat to pea production, and improved resistance to this disease is needed. Nodal resistance in plants is a phenomenon where a fungal infection is prevented from passing through a node, and the infection is limited to an internode region. Nodal resistance has been observed in some pathosystems such as the pea (Pisum sativum L.)‐S. sclerotiorum pathosystem. In addition to nodal resistance, different pea lines display different levels of stem lesion size restriction, referred to as lesion resistance. It is unclear whether the genetics of lesion resistance and nodal resistance are identical or different. This study applied genome‐wide association studies (GWAS) and RNA‐Seq to understand the genetic makeup of these two types of resistance. The time series RNA‐Seq experiment consisted of two pea lines (the susceptible ‘Lifter’ and the partially resistant PI 240515), two treatments (mock inoculated samples and S. sclerotiorum‐inoculated samples), and three time points (12, 24, and 48 hr post inoculation). Integrated results from GWAS and RNA‐Seq analyses identified different redox‐related transcripts for lesion and nodal resistances. A transcript encoding a glutathione S‐transferase was the only shared resistance variant for both phenotypes. There were more leucine rich‐repeat containing transcripts found for lesion resistance, while different candidate resistance transcripts such as a VQ motif‐containing protein and a myo‐inositol oxygenase were found for nodal resistance. This study demonstrated the robustness of combining GWAS and RNA‐Seq for identifying white mold resistance in pea, and results suggest different genetics underlying lesion and nodal resistance.

Highlights

Sclerotinia sclerotiorum (Lib.) de Bary, the causal agent of white mold disease, is one of the most destructive plant pathogens worldwide
Studies searching for plant resistance to S. sclerotiorum have found quantitative interactions (McCaghey et al, 2017), and potential resistance genes included those with functions to maintain reactive oxygen species (ROS) and redox stresses during S. sclerotiorum infection (Girard et al, 2017; Ranjan et al, 2017; Zhou, Sun, & Xing, 2013)
We localized significant single nucleotide polymorphisms (SNPs) identified from genome-wide association studies (GWAS) using a de novo transcriptome

Summary

| INTRODUCTION

Sclerotinia sclerotiorum (Lib.) de Bary, the causal agent of white mold disease, is one of the most destructive plant pathogens worldwide. Transcriptomics and differential expression (DE) analysis using RNA-Seq have become a standard approach to identifying resistance genes for white mold, and studies have applied this approach to oilseed rape (Brassica napus) and pea (Girard et al, 2017; Seifbarghi et al, 2017; Zhuang, McPhee, Coram, Peever, & Chilvers, 2012). RNA-Seq and GWAS both have their advantages, and combining them provides a powerful tool to discover active genes that express in response to treatments, and genetic diversity and SNPs associated with the treatment This combined strategy has been applied to understand white mold resistance and yields in B. napus (Lu et al, 2017; Wei et al, 2016) and soybean (Wen et al, 2018), but not in pea. Because genes that can be found by both GWAS and RNA-Seq will have higher potential in contributing to white mold resistance, this study aimed to understand and compare the genetics of lesion and nodal resistance by applying both GWAS and RNA-Seq approaches in the pea-S. sclerotiorum pathosystem

| MATERIALS AND METHODS

| RESULTS

| DISCUSSION

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Findings

CONFLICT OF INTEREST