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Cited 114 time in webofscience Cited 134 time in scopus
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Epigenetic switch from repressive to permissive chromatin in response to cold stressopen access

Authors
Park, JunghoonLim, Chae JinShen, MingzhePark, Hee JinCha, Joon-YungIniesto, ElisaRubio, VicenteMengiste, TesfayeZhu, Jian-KangBressan, Ray A.Lee, Sang YeolLee, Byeong-haJin, Jing BoPardo, Jose M.Kim, Woe-YeonYun, Dae-Jin
Issue Date
5-Jun-2018
Publisher
NATL ACAD SCIENCES
Keywords
histone acetylation; derepression; cold stress response; CUL4-based E3 ligase; HOS15
Citation
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, v.115, no.23, pp.E5400 - E5409
Indexed
SCIE
SCOPUS
Journal Title
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume
115
Number
23
Start Page
E5400
End Page
E5409
URI
https://scholarworks.bwise.kr/gnu/handle/sw.gnu/11561
DOI
10.1073/pnas.1721241115
ISSN
0027-8424
Abstract
Switching from repressed to active status in chromatin regulation is part of the critical responses that plants deploy to survive in an ever-changing environment. We previously reported that HOS15, a WD40-repeat protein, is involved in histone deacetylation and cold tolerance in Arabidopsis. However, it remained unknown how HOS15 regulates cold responsive genes to affect cold tolerance. Here, we show that HOS15 interacts with histone deacetylase 2C (HD2C) and both proteins together associate with the promoters of cold-responsive COR genes, COR15A and COR47. Cold induced HD2C degradation is mediated by the CULLIN4 (CUL4)-based E3 ubiquitin ligase complex in which HOS15 acts as a substrate receptor. Interference with the association of HD2C and the COR gene promoters by HOS15 correlates with increased acetylation levels of histone H3. HOS15 also interacts with CBF transcription factors to modulate cold-induced binding to the COR gene promoters. Our results here demonstrate that cold induces HOS15-mediated chromatin modifications by degrading HD2C. This switches the chromatin structure status and facilitates recruitment of CBFs to the COR gene promoters. This is an apparent requirement to acquire cold tolerance.
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