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Cited 25 time in webofscience Cited 25 time in scopus
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HOS15 is a transcriptional corepressor of NPR1-mediated gene activation of plant immunityopen access

Authors
Shen, MingzheLim, Chae JinPark, JunghoonKim, Jeong EunBaek, DongwonNam, JaesungLee, Sang YeolPardo, Jose M.Kim, Woe-YeonMackey, DavidYun, 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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