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

TitleInducible nucleosome depletion at OREBP-binding-sites by hypertonic stress
Authors
Issue Date2009
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
Citation
Plos One, 2009, v. 4 n. 12 How to Cite?
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.
Persistent Identifierhttp://hdl.handle.net/10722/124487
ISSN
2014 Impact Factor: 3.234
2014 SCImago Journal Rankings: 1.300
PubMed Central ID
ISI Accession Number ID
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.

References

 

DC FieldValueLanguage
dc.contributor.authorTong, EHYen_HK
dc.contributor.authorGuo, JJen_HK
dc.contributor.authorXu, SXen_HK
dc.contributor.authorMak, Ken_HK
dc.contributor.authorChung, SKen_HK
dc.contributor.authorChung, SSMen_HK
dc.contributor.authorHuang, ALen_HK
dc.contributor.authorKo, BCBen_HK
dc.date.accessioned2010-10-31T10:37:09Z-
dc.date.available2010-10-31T10:37:09Z-
dc.date.issued2009en_HK
dc.identifier.citationPlos One, 2009, v. 4 n. 12en_HK
dc.identifier.issn1932-6203en_HK
dc.identifier.urihttp://hdl.handle.net/10722/124487-
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.en_HK
dc.languageengen_HK
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.actionen_HK
dc.relation.ispartofPLoS ONEen_HK
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 stressen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1932-6203&volume=4&issue=12, article no. e8435&spage=&epage=&date=2009&atitle=Inducible+nucleosome+depletion+at+OREBP-binding-sites+by+hypertonic+stress-
dc.identifier.emailChung, SK: skchung@hkucc.hku.hken_HK
dc.identifier.emailChung, SSM: smchung@hkucc.hku.hken_HK
dc.identifier.authorityChung, SK=rp00381en_HK
dc.identifier.authorityChung, SSM=rp00376en_HK
dc.description.naturepublished_or_final_versionen_US
dc.identifier.doi10.1371/journal.pone.0008435en_HK
dc.identifier.pmid20041176en_HK
dc.identifier.pmcidPMC2793017-
dc.identifier.scopuseid_2-s2.0-77949517845en_HK
dc.identifier.hkuros182033en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77949517845&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume4en_HK
dc.identifier.issue12en_HK
dc.identifier.isiWOS:000273104000005-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridTong, EHY=7006335224en_HK
dc.identifier.scopusauthoridGuo, JJ=23766904300en_HK
dc.identifier.scopusauthoridXu, SX=14026187000en_HK
dc.identifier.scopusauthoridMak, K=35748734500en_HK
dc.identifier.scopusauthoridChung, SK=7404292976en_HK
dc.identifier.scopusauthoridChung, SSM=14120761600en_HK
dc.identifier.scopusauthoridHuang, AL=35748798900en_HK
dc.identifier.scopusauthoridKo, BCB=7102833927en_HK

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