Lauric Acid Induces Apoptosis of Rice Sheath Blight Disease Caused by Rhizoctonia solani by Affecting Fungal Fatty Acid Metabolism and Destroying the Dynamic Equilibrium of Reactive Oxygen Species

Jian Wang,Tingchi Wen,Chenglong Yang,Xiaomao Wu,Rongyu Li,Lei Han,Li Ming,Xiaolong Yao,Xianfeng Hu

doi:10.3390/jof8020153

Abstract

Rice sheath blight, caused by Rhizoctonia solani, is one of the major rice diseases. In order to better understand the inhibitory mechanism of lauric acid on the disease, RNA sequencing (RNA-Seq) was used to analyze the transcriptome changes in Rhizoctonia solani treated with lauric acid for 3 h, 6 h, 18 h, and 24 h, including 2306 genes; 1994 genes; 2778 genes; and 2872 genes. Based on gene ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses, we found that protein processing in endoplasmic reticulum (KO04141), carbon metabolism (KO01200), and starch and sucrose metabolism were significantly enriched. Most oxidoreductase, dehydrogenase, reductase, and transferase genes are downregulated in this process. Lauric acid can affect ergosterol content, mitochondrial membrane potential collapse, hydrogen peroxide content, electrolyte leakage, reactive oxygen species balance, and can induce endoplasmic reticulum (ER) stress. Lauric acid also increased the expression levels of ER chaperone glucose regulatory protein Grp78 (BIP), protein disulfide isomerase (PDI), and Calpain (CNX), and decreased the expression levels of HSP40, HSP70, and HSP90 genes. Lauric acid affected the ergosterol content in the cell membrane of R. solani, which induces ER stress and increases the BiP level to induce the apoptosis of Rhizoctonia solani. These results indicated that lauric acid could be used to control rice sheath blight.

Highlights

Rice sheath blight, a soil-borne fungal disease [1,2], is caused by Rhizoctonia solani (R. solani) infection, and is one of the three major diseases of rice; the second most common disease next to rice blast
We found that lauric acid can oxidize the membrane system, destroy the integrity of the cell membrane, and enhance the permeability of the membrane in R. solani, affecting mycelium growth
Our results showed that lauric acid induced the upregulation of glucanase and fatty acid metabolism-related genes, increased the amount of ergosterol in the cell membrane, led to cell membrane damage, and downregulated cytochrome oxidase and upregulated iron reductase, resulting in the accumulation of intracellular Reactive oxygen species (ROS) (H2O2)

Summary

Introduction

A soil-borne fungal disease [1,2], is caused by Rhizoctonia solani (R. solani) infection, and is one of the three major diseases of rice; the second most common disease next to rice blast. The asexual state of the pathogen is R. solani, and the sexual state is Thanatephorus cucumeris [3]. It occurs globally in rice plantations in the form of hyphae or sclerotium, which reduces the yield of rice by 10–30%, and could reach up to 50% in severe disease areas [4]. The pathogen has a wide host range, and the sclerotia has tenacious vitality, reaching a germination rate of up to 12%, even after 11 years [5,6], making this pathogen difficult to control. No immune or highly resistant varieties have been found in rice sheath blight resistance breeding, which leads to an upward trend in the incidence rate [7]. It is very important and urgent to find effective measures to prevent and control rice sheath blight

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