OsEIL2 balances rice immune responses against (hemi)biotrophic and necrotrophic pathogens via the salicylic acid and jasmonic acid synergism

Author:

Zhao Yudan1,Zhu Xiaoying1,Shi Cheng‐Min2,Xu Guojuan1,Zuo Shimin3,Shi Yanlong1,Cao Wenlei3ORCID,Kang Houxiang1,Liu Wende1ORCID,Wang Ruyi1,Ning Yuese1,Wang Guo‐Liang4ORCID,Wang Xuli1ORCID

Affiliation:

1. State Key Laboratory for Biology of Plant Diseases and Insect Pests, Institute of Plant Protection Chinese Academy of Agricultural Sciences Beijing 100193 China

2. State Key Laboratory of North China Crop Improvement and Regulation, College of Plant Protection Hebei Agricultural University Baoding 071001 China

3. Key Laboratory of Plant Functional Genomics of the Ministry of Education, Jiangsu Key Laboratory of Crop Genomics and Molecular Breeding Agricultural College of Yangzhou University Yangzhou 225009 China

4. Department of Plant Pathology The Ohio State University Columbus OH 43210 USA

Abstract

Summary Plants typically activate distinct defense pathways against various pathogens. Heightened resistance to one pathogen often coincides with increased susceptibility to another pathogen. However, the underlying molecular basis of this antagonistic response remains unclear. Here, we demonstrate that mutants defective in the transcription factor ETHYLENE‐INSENSITIVE 3‐LIKE 2 (OsEIL2) exhibited enhanced resistance to the biotrophic bacterial pathogen Xanthomonas oryzae pv oryzae and to the hemibiotrophic fungal pathogen Magnaporthe oryzae, but enhanced susceptibility to the necrotrophic fungal pathogen Rhizoctonia solani. Furthermore, necrotroph‐induced OsEIL2 binds to the promoter of OsWRKY67 with high affinity, leading to the upregulation of salicylic acid (SA)/jasmonic acid (JA) pathway genes and increased SA/JA levels, ultimately resulting in enhanced resistance. However, biotroph‐ and hemibiotroph‐induced OsEIL2 targets OsERF083, resulting in the inhibition of SA/JA pathway genes and decreased SA/JA levels, ultimately leading to reduced resistance. Our findings unveil a previously uncharacterized defense mechanism wherein two distinct transcriptional regulatory modules differentially mediate immunity against pathogens with different lifestyles through the transcriptional reprogramming of phytohormone pathway genes.

Funder

National Key Research and Development Program of China

National Natural Science Foundation of China

National Transgenic Science and Technology Program

Publisher

Wiley

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