HOS15 is a transcriptional corepressor of NPR1-mediated gene activation of plant immunityopen access
- Authors
- Shen, Mingzhe; Lim, Chae Jin; Park, Junghoon; Kim, Jeong Eun; Baek, Dongwon; Nam, Jaesung; Lee, Sang Yeol; Pardo, Jose M.; Kim, Woe-Yeon; Mackey, David; Yun, Dae-Jin
- Issue Date
- 1-Dec-2020
- Publisher
- National Academy of Sciences
- Keywords
- HOS15; NPR1; ubiquitin ligase; corepressor; plant immunity
- Citation
- Proceedings of the National Academy of Sciences of the United States of America, v.117, no.48, pp 30805 - 30815
- Pages
- 11
- Indexed
- SCIE
SCOPUS
- Journal Title
- Proceedings of the National Academy of Sciences of the United States of America
- Volume
- 117
- Number
- 48
- Start Page
- 30805
- End Page
- 30815
- URI
- https://scholarworks.gnu.ac.kr/handle/sw.gnu/5803
- DOI
- 10.1073/pnas.2016049117
- ISSN
- 0027-8424
1091-6490
- Abstract
- Transcriptional regulation is a complex and pivotal process in living cells. HOS15 is a transcriptional corepressor. Although transcriptional repressors generally have been associated with inactive genes, increasing evidence indicates that, through poorly understood mechanisms, transcriptional corepressors also associate with actively transcribed genes. Here, we show that HOS15 is the substrate receptor for an SCF/CUL1 E3 ubiquitin ligase complex (SCFHOS15) that negatively regulates plant immunity by destabilizing transcriptional activation complexes containing NPR1 and associated transcriptional activators. In unchallenged conditions, HOS15 continuously eliminates NPR1 to prevent inappropriate defense gene expression. Upon defense activation, HOS15 preferentially associates with phosphorylated NPR1 to stimulate rapid degradation of transcriptionally active NPR1 and thus limit the extent of defense gene expression. Our findings indicate that HOS15-mediated ubiquitination and elimination of NPR1 produce effects contrary to those of CUL3-containing ubiquitin ligase that coactivate defense gene expression. Thus, HOS15 plays a key role in the dynamic regulation of preand postactivation host defense.
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