Osa-miR398b boosts H 2 O 2 production and rice blast disease-resistance via multiple superoxide dismutases

• Published in: The New phytologist Vol. 222; no. 3; pp. 1507 - 1522
• Main Authors: Li, Yan, Cao, Xiao-Long, Zhu, Yong, Yang, Xue-Mei, Zhang, Kai-Ni, Xiao, Zhi-Yuan, Wang, He, Zhao, Jing-Hao, Zhang, Ling-Li, Li, Guo-Bang, Zheng, Ya-Ping, Fan, Jing, Wang, Jing, Chen, Xiao-Qiong, Wu, Xian-Jun, Zhao, Ji-Qun, Dong, Oliver Xiaoou, Chen, Xue-Wei, Chern, Mawsheng, Wang, Wen-Ming
• Format: Journal Article
• Language: English
• Published: England 01.05.2019
• Subjects: Disease Resistance; Down-Regulation; Gene Expression Regulation, Plant; Hydrogen Peroxide - metabolism; Magnaporthe; MicroRNAs - genetics; MicroRNAs - metabolism; Models, Biological; Mutation - genetics; Oryza - genetics; Oryza - metabolism; Oryza - microbiology; Plant Diseases - microbiology; Reactive Oxygen Species - metabolism; Superoxide Dismutase - metabolism; Cu/Zn-Superoxidase Dismutase; enzyme activity; Magnaporthe oryzae; miR398b; H2O2; rice resistance; Superoxide Dismutase
• ISSN: 0028-646X; 1469-8137
• DOI: 10.1111/nph.15678

miRNAs contribute to plant resistance against pathogens. Previously, we found that the function of miR398b in immunity in rice differs from that in Arabidopsis. However, the underlying mechanisms are unclear. In this study, we characterized the mutants of miR398b target genes and demonstrated that multiple superoxide dismutase genes contribute to miR398b-regulated rice immunity against the blast fungus Magnaporthe oryzae. Out of the four target genes of miR398b, mutations in Cu/Zn-Superoxidase Dismutase1 (CSD1), CSD2 and Os11g09780 (Superoxide DismutaseX, SODX) led to enhanced resistance to M. oryzae and increased hydrogen peroxide (H O ) accumulation. By contrast, mutations in Copper Chaperone for Superoxide Dismutase (CCSD) resulted in enhanced susceptibility. Biochemical studies revealed that csd1, csd2 and sodx displayed altered expression of CSDs and other superoxide dismutase (SOD) family members, leading to increased total SOD enzyme activity that positively contributed to higher H O production. By contrast, the ccsd mutant showed CSD protein deletion, resulting in decreased CSD and total SOD enzyme activity. Our results demonstrate the roles of different SODs in miR398b-regulated resistance to rice blast disease, and uncover an integrative regulatory network in which miR398b boosts total SOD activity to upregulate H O concentration and thereby improve disease resistance.