| Literature DB >> 27978435 |
Quanyuan You1, Keran Zhai1, Donglei Yang2, Weibing Yang3, Jingni Wu3, Junzhong Liu1, Wenbo Pan4, Jianjun Wang5, Xudong Zhu6, Yikun Jian7, Jiyun Liu3, Yingying Zhang3, Yiwen Deng3, Qun Li3, Yonggen Lou7, Qi Xie4, Zuhua He8.
Abstract
Programmed cell death (PCD) and immunity in plants are tightly controlled to promote antimicrobial defense while preventing autoimmunity. However, the mechanisms contributing to this immune homeostasis are poorly understood. Here, we isolated a rice mutant ebr1 (enhanced blight and blast resistance 1) that shows enhanced broad-spectrum bacterial and fungal disease resistance, but displays spontaneous PCD, autoimmunity, and stunted growth. EBR1 encodes an E3 ubiquitin ligase that interacts with OsBAG4, which belongs to the BAG (Bcl-2-associated athanogene) family that functions in cell death, growth arrest, and immune responses in mammals. EBR1 directly targets OsBAG4 for ubiquitination-mediated degradation. Elevated levels of OsBAG4 in rice are necessary and sufficient to trigger PCD and enhanced disease resistance to pathogenic infection, most likely by activating pathogen-associated molecular patterns-triggered immunity (PTI). Together, our study suggests that an E3-BAG module orchestrates innate immune homeostasis and coordinates the trade-off between defense and growth in plants.Entities:
Keywords: BAG protein; E3 ubiquitin ligase; autoimmunity; broad-spectrum disease resistance; defense cost; molecular module; programmed cell death; rice
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Year: 2016 PMID: 27978435 DOI: 10.1016/j.chom.2016.10.023
Source DB: PubMed Journal: Cell Host Microbe ISSN: 1931-3128 Impact factor: 21.023