Author:
ZHANG Xiangyue,FENG Zili,ZHAO Lihong,LIU Shichao,WEI Feng,SHI Yongqiang,FENG Hongjie,ZHU Heqin
Abstract
Abstract
Background
Verticillium wilt, caused by the soil-borne fungus of Verticillium dahliae Kleb., is one of the most devastating diseases of cotton. The complex mechanism underlying cotton resistance to Verticillium wilt remains uncharacterized. Identifying an endogenous resistance gene may be helpful to control this disease. Previous studies revealed that succinate dehydrogenase (SDH) is involved in reactive oxygen species (ROS)-induced stress signaling pathway that is likely to be triggered by salicylic acid (SA). Here, through the metabolomics and differential expression analyses in wilt-inoculated cotton (Gossypium hirsutum), we noticed that GhSDH1–1 gene in cotton may play an important role in the resistance to V. dahlia. Then we reported GhSDH1–1 gene and its functional analysis in relation to the resistance of cotton to V. dahliae.
Results
The GhSDH1–1 gene in cotton root was significantly up-regulated after V. dahlia inoculation, and its expression level peaked at 12 and 24 h post-infection. SA can also induce the up-regulation of GhSDH1–1. Additionally, the functional analysis showed that GhSDH1–1-silenced cotton was more susceptible to V. dahliae than the control because of the significant decrease in abundance of immune-related molecules and severe damage to the SA-signaling pathway. In Arabidopsis thaliana, high expression of GhSDH1–1 conferred high resistance to V. dahliae. Arabidopsis that overexpressed GhSDH1–1 had higher resistance to V. dahliae infection compared with the wild-type.
Conclusions
Our findings provide new insights into the role of GhSDH1–1; it positively regulates cotton resistance to Verticillium wilt. The regulatory mechanism of GhSDH1–1 is closely related to SA-related signaling pathway.
Funder
National Natural Science Foundation of China
Publisher
Springer Science and Business Media LLC
Subject
Agricultural and Biological Sciences (miscellaneous),Biochemistry, Genetics and Molecular Biology (miscellaneous)
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