ROS and trehalose regulate sclerotial development in Rhizoctonia solani AG-1 IA

被引:28
|
作者
Wang, Chenjiaozi [1 ]
Pi, Lei [1 ]
Jiang, Shaofeng [1 ]
Yang, Mei [1 ]
Shu, Canwei [1 ]
Zhou, Erxun [1 ]
机构
[1] South China Agr Univ, Dept Plant Pathol, Guangdong Prov Key Lab Microbial Signals & Dis Co, Guangzhou 510642, Guangdong, Peoples R China
基金
中国国家自然科学基金;
关键词
Rhizoctonia solani AG-1 IA; Rice sheath blight; ROS; Sclerotial development; Trehalose; RICE SHEATH BLIGHT; THIOL REDOX STATE; OXIDATIVE STRESS; DIFFERENTIATION; PATHOGEN; GROWTH; BIOSYNTHESIS; METABOLISM; RESISTANCE; VIRULENCE;
D O I
10.1016/j.funbio.2018.02.003
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Rhizoctonia solani AG-1 IA is the causal agent of rice sheath blight (RSB) and causes severe economic losses in rice-growing regions around the world. The sclerotia play an important role in the disease cycle of RSB. In this study, we report the effects of reactive oxygen species (ROS) and trehalose on the sclerotial development of R. solani AG-1 IA. Correlation was found between the level of ROS in R. solani AG-1 IA and sclerotial development. Moreover, we have shown the change of ROS-related enzymatic activities and oxidative burst occurs at the sclerotial initial stage. Six genes related to the ROS scavenging system were quantified in different sclerotial development stages by using quantitative RT-PCR technique, thereby confirming differential gene expression. Fluorescence microscopy analysis of ROS content in mycelia revealed that ROS were predominantly produced at the hyphal branches during the sclerotial initial stage. Furthermore, exogenous trehalose had a significant inhibitory effect on the activities of ROSrelated enzymes and oxidative burst and led to a reduction in sclerotial dry weight. Taken together, the findings suggest that ROS has a promoting effect on the development of sclerotia, whereas trehalose serves as an inhibiting factor to sclerotial development in R. solani AG-i IA. (C) 2018 British Mycological Society. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码:322 / 332
页数:11
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