The hypersensitive induced reaction 3 (HIR3) gene contributes to plant basal resistance via an EDS1 and salicylic acid-dependent pathway
文献类型: 外文期刊
第一作者: Li, Saisai
作者: Li, Saisai;Wu, Xinyang;Chen, Jianping;Li, Saisai;Zhao, Jinping;Zhang, Hehong;Wu, Xinyang;Lu, Yuwen;Peng, Jiejun;Sun, Zongtao;Lin, Lin;Zheng, Hongying;Chen, Jianping;Yan, Fei;Li, Saisai;Zhao, Jinping;Zhang, Hehong;Wu, Xinyang;Lu, Yuwen;Peng, Jiejun;Sun, Zongtao;Lin, Lin;Zheng, Hongying;Chen, Jianping;Yan, Fei;Zhai, Yushan;Yuan, Quan;Lu, Yuwen;Peng, Jiejun;Sun, Zongtao;Lin, Lin;Zheng, Hongying;Chen, Jianping;Yan, Fei
作者机构:
关键词: hypersensitive reaction; hypersensitive induced reaction gene; salicylic acid; rice stripe virus; plant basal defense
期刊名称:PLANT JOURNAL ( 影响因子:6.417; 五年影响因子:7.627 )
ISSN: 0960-7412
年卷期: 2019 年 98 卷 5 期
页码:
收录情况: SCI
摘要: The hypersensitive-induced reaction (HIR) gene family is associated with the hypersensitive response (HR) that is a part of the plant defense system against bacterial and fungal pathogens. The involvement of HIR genes in response to viral pathogens has not yet been studied. We now report that the HIR3 genes of Nicotiana benthamiana and Oryza sativa (rice) were upregulated following rice stripe virus (RSV) infection. Silencing of HIR3s in N. benthamiana resulted in an increased accumulation of RSV RNAs, whereas overexpression of HIR3s in N. benthamiana or rice reduced the expression of RSV RNAs and decreased symptom severity, while also conferring resistance to Turnip mosaic virus, Potato virus X, and the bacterial pathogens Pseudomonas syringae and Xanthomonas oryzae. Silencing of HIR3 genes in N. benthamiana reduced the content of salicylic acid (SA) and was accompanied by the downregulated expression of genes in the SA pathway. Transient expression of the two HIR3 gene homologs from N. benthamiana or the rice HIR3 gene in N. benthamiana leaves caused cell death and an accumulation of SA, but did not do so in EDS1-silenced plants or in plants expressing NahG. The results indicate that HIR3 contributes to plant basal resistance via an EDS1- and SA-dependent pathway.
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