Antagonistic control of rice immunity against distinct pathogens by the two transcription modules via salicylic acid and jasmonic acid pathways
文献类型： 外文期刊
作者： Zhu, Xiaoying 1 ; Zhao, Yudan 1 ; Shi, Cheng-Min 1 ; Xu, Guojuan 1 ; Wang, Nana 1 ; Zuo, Shimin 3 ; Ning, Yuese 1 ; Kang, Houxiang 1 ; Liu, Wende 1 ; Wang, Ruyi 1 ; Yan, Shuangyong 4 ; Wang, Guo-Liang 5 ; Wang, Xuli 1 ;
作者机构： 1.Chinese Acad Agr Sci, Inst Plant Protect, State Key Lab Biol Plant Dis & Insect Pests, Beijing 100193, Peoples R China
2.Hebei Agr Univ, Coll Plant Protect, State Key Lab North China Crop Improvement & Regul, Baoding 071001, Peoples R China
3.Yangzhou Univ, Minist Educ, Agr Coll, Jiangsu Key Lab Crop Genom & Mol Breeding,Key Lab, Yangzhou 225009, Peoples R China
4.Tianjin Acad Agr Sci, Inst Crop Res, Tianjin 300381, Peoples R China
5.Ohio State Univ, Dept Plant Pathol, Columbus, OH 43210 USA
期刊名称：DEVELOPMENTAL CELL （ 影响因子：10.7； 五年影响因子：11.5 ）
ISSN： 1534-5807
年卷期： 2024 年 59 卷 12 期
页码：
收录情况： SCI
摘要： Although the antagonistic effects of host resistance against biotrophic and necrotrophic pathogens have been documented in various plants, the underlying mechanisms are unknown. Here, we investigated the antagonistic resistance mediated by the transcription factor ETHYLENE-INSENSITIVE3-LIKE 3 (OsEIL3) in rice. The Oseil3 mutant confers enhanced resistance to the necrotroph Rhizoctonia solani but greater susceptibility to the hemibiotroph Magnaporthe oryzae and biotroph Xanthomonas oryzae pv. oryzae . OsEIL3 directly activates OsERF040 transcription while repressing OsWRKY28 transcription. The infection of R. solani and M. oryzae or Xoo influences the extent of binding of OsEIL3 to OsWRKY28 and OsERF040 promoters, resulting in the repression or activation of both salicylic acid (SA)- and jasmonic acid (JA) -dependent pathways and enhanced susceptibility or resistance, respectively. These results demonstrate that the distinct effects of plant immunity to different pathogen types are determined by two transcription factor modules that control transcriptional reprogramming and the SA and JA pathways.
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