Article: Inducible nucleosome depletion at OREBP-binding-sites by hypertonic stress

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TitleInducible nucleosome depletion at OREBP-binding-sites by hypertonic stress
AuthorsTong, EHY1 3
Guo, JJ2
Xu, SX3
Mak, K1
Chung, SK1
Chung, SSM1
Huang, AL2
Ko, BCB3
Issue Date2009
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
CitationPlos One, 2009, v. 4 n. 12 [How to Cite?]
DOI: http://dx.doi.org/10.1371/journal.pone.0008435
AbstractBackground: Osmotic Response Element-Binding Protein (OREBP), also known as TonEBP or NFAT5, is a unique transcription factor. It is hitherto the only known mammalian transcription factor that regulates hypertonic stress-induced gene transcription. In addition, unlike other monomeric members of the NFAT family, OREBP exists as a homodimer and it is the only transcription factor known to bind naked DNA targets by complete encirclement in vitro. Nevertheless, how OREBP interacts with target DNA, also known as ORE/TonE, and how it elicits gene transcription in vivo, remains unknown. Methodology: Using hypertonic induction of the aldose reductase (AR) gene activation as a model, we showed that OREs contained dynamic nucleosomes. Hypertonic stress induced a rapid and reversible loss of nucleosome(s) around the OREs. The loss of nucleosome(s) was found to be initiated by an OREBP-independent mechanism, but was significantly potentiated in the presence of OREBP. Furthermore, hypertonic induction of AR gene was associated with an OREBPdependent hyperacetylation of histones that spanned the 59 upstream sequences and at least some exons of the gene. Nevertheless, nucleosome loss was not regulated by the acetylation status of histone. Significance: Our findings offer novel insights into the mechanism of OREBP-dependent transcriptional regulation and provide a basis for understanding how histone eviction and transcription factor recruitment are coupled. © 2009 Tong et al.
ISSN1932-6203
2011 Impact Factor: 4.092
2011 SCImago Journal Rankings: 0.519
DOIhttp://dx.doi.org/10.1371/journal.pone.0008435
PubMed Central IDPMC2793017
ReferencesReferences in Scopus
DC Field
Value
dc.contributor.authorTong, EHY
dc.contributor.authorGuo, JJ
dc.contributor.authorXu, SX
dc.contributor.authorMak, K
dc.contributor.authorChung, SK
dc.contributor.authorChung, SSM
dc.contributor.authorHuang, AL
dc.contributor.authorKo, BCB
dc.date.accessioned2010-10-31T10:37:09Z
dc.date.available2010-10-31T10:37:09Z
dc.date.issued2009
dc.description.abstractBackground: Osmotic Response Element-Binding Protein (OREBP), also known as TonEBP or NFAT5, is a unique transcription factor. It is hitherto the only known mammalian transcription factor that regulates hypertonic stress-induced gene transcription. In addition, unlike other monomeric members of the NFAT family, OREBP exists as a homodimer and it is the only transcription factor known to bind naked DNA targets by complete encirclement in vitro. Nevertheless, how OREBP interacts with target DNA, also known as ORE/TonE, and how it elicits gene transcription in vivo, remains unknown. Methodology: Using hypertonic induction of the aldose reductase (AR) gene activation as a model, we showed that OREs contained dynamic nucleosomes. Hypertonic stress induced a rapid and reversible loss of nucleosome(s) around the OREs. The loss of nucleosome(s) was found to be initiated by an OREBP-independent mechanism, but was significantly potentiated in the presence of OREBP. Furthermore, hypertonic induction of AR gene was associated with an OREBPdependent hyperacetylation of histones that spanned the 59 upstream sequences and at least some exons of the gene. Nevertheless, nucleosome loss was not regulated by the acetylation status of histone. Significance: Our findings offer novel insights into the mechanism of OREBP-dependent transcriptional regulation and provide a basis for understanding how histone eviction and transcription factor recruitment are coupled. © 2009 Tong et al.
dc.description.naturepublished_or_final_version
dc.identifier.citationPlos One, 2009, v. 4 n. 12 [How to Cite?]
DOI: http://dx.doi.org/10.1371/journal.pone.0008435
dc.identifier.doihttp://dx.doi.org/10.1371/journal.pone.0008435
dc.identifier.hkuros182033
dc.identifier.isiWOS:000273104000005
Funding AgencyGrant Number
Research Grant CouncilCUHK 7327/04M
CUHK 466108
Chinese University of Hong Kong Direct2041317
Funding Information:

This work was supported by the Research Grant Council Grants CUHK 7327/04M, CUHK 466108 and by the Chinese University of Hong Kong Direct Grant for Research 2041317 ( to B. C. B. K). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

dc.identifier.issn1932-6203
2011 Impact Factor: 4.092
2011 SCImago Journal Rankings: 0.519
dc.identifier.issue12
dc.identifier.openurl
dc.identifier.pmcidPMC2793017
dc.identifier.pmid20041176
dc.identifier.scopuseid_2-s2.0-77949517845
dc.identifier.urihttp://hdl.handle.net/10722/124487
dc.identifier.volume4
dc.languageeng
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
dc.publisher.placeUnited States
dc.relation.ispartofPLoS ONE
dc.relation.referencesReferences in Scopus
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License
dc.subject.meshAcetylation - drug effects
dc.subject.meshHypertonic Solutions - pharmacology
dc.subject.meshNFATC Transcription Factors - metabolism
dc.subject.meshNucleosomes - metabolism
dc.subject.meshStress, Physiological - drug effects
dc.titleInducible nucleosome depletion at OREBP-binding-sites by hypertonic stress
dc.typeArticle
Author Affiliations
  1. The University of Hong Kong
  2. Chongqing University of Medical Sciences
  3. Chinese University of Hong Kong