期刊
CELL
卷 182, 期 5, 页码 1093-+出版社
CELL PRESS
DOI: 10.1016/j.cell.2020.07.016
关键词
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资金
- National Institutes of Health [NIH 1R35GM118036]
- Howard Hughes Medical Institute
- Vaadia-BARD postdoctoral fellowship from the United States-Israel Binational Agricultural Research and Development Fund [FI-477-2013]
In plants, pathogen effector-triggered immunity (ETI) often leads to programmed cell death, which is restricted by NPR1, an activator of systemic acquired resistance. However, the biochemical activities of NPR1 enabling it to promote defense and restrict cell death remain unclear. Here we show that NPR1 promotes cell survival by targeting substrates for ubiquitination and degradation through formation of salicylic acid-induced NPR1 condensates (SINCs). SINCs are enriched with stress response proteins, including nucleotide-binding leucine-rich repeat immune receptors, oxidative and DNA damage response proteins, and protein quality control machineries. Transition of NPR1 into condensates is required for formation of the NPR1-Cullin 3 E3 ligase complex to ubiquitinate SINC-localized substrates, such as EDS1 and specific WRKY transcription factors, and promote cell survival during ETI. Our analysis of SINCs suggests that NPR1 is centrally integrated into the cell death or survival decisions in plant immunity by modulating multiple stress-responsive processes in this quasi-organelle.
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