The DOI matches its Crossref record; 77 of the 77 references it cites were found in a registry or an index.
Formation of NPR1 Condensates Promotes Cell Survival during the Plant Immune Response
Open accessAbstract
SUMMARY 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 both 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 the 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/survival decisions in plant immunity by modulating multiple stress-responsive processes in this quasi organelle.
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Reuter, L., Schmidt, T., Manishankar, P., Throm, C., Keicher, J., Bock, A., Droste-Borel, I., & Oecking, C. (2021) · Nature Communications · doi:10.1038/s41467-021-26332-6 · Cited by 56
The tRNA thiolation-mediated translational control is essential for plant immunity
Zheng, X., Chen, H., Deng, Z., Wu, Y., Zhong, L., Wu, C., Yu, X., Chen, Q., & Yan, S. (2024) · eLife · doi:10.7554/elife.93517 · Cited by 19
Metadata
- Authors
- Zavaliev, R., Mohan, R., Chen, T., & Dong, X.
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2020-09
- Volume
- 182
- Issue
- 5
- Pages
- 1093-1108.e18
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W3049197258
- Cited by
- 365
- References
- 77
- FWCI
- 22.68
- Type
- journal article
- Language
- en
- Open access
- bronze
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