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Article: Epigenetic inheritance of cell differentiation status

TitleEpigenetic inheritance of cell differentiation status
Authors
Issue Date2008
PublisherLandes Bioscience. The Journal's web site is located at http://www.landesbioscience.com/journals/cc
Citation
Cell Cycle, 2008, v. 7 n. 9, p. 1173-1177 How to Cite?
AbstractEpigenetic modifications influence gene expression pattern and provide a unique signature of a cell differentiation status. Without external stimuli or signalling events, this cell identity remains stable and unlikely to change over many cell divisions. The epigenetic signature of a particular cell fate therefore needs to be replicated faithfully in daughter cells; otherwise a cell lineage cannot be maintained. However, the mechanism of transmission of cellular memory from mother to daughter cells remains unclear. It has been suggested that the inheritance of an active or silent gene state involves different kinds of epigenetic mechanisms, e.g., DNA methylation, histone modifications, replacement of histone variants, Polycomb group (PcG) and Trithorax group (TrxG) proteins. Emerging evidence supports the role of histone variant H3.3 in maintaining an active gene status and in remodelling nucleosomal composition. Here we discuss some recent findings on the propagation of epigenetic memory and propose a model for the inheritance of an active gene state through the interaction of H3.3 with other epigenetic components. ©2008 Landes Bioscience.
Persistent Identifierhttp://hdl.handle.net/10722/148564
ISSN
2015 Impact Factor: 3.952
2015 SCImago Journal Rankings: 2.244
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorNg, RKen_US
dc.contributor.authorGurdon, JBen_US
dc.date.accessioned2012-05-29T06:13:45Z-
dc.date.available2012-05-29T06:13:45Z-
dc.date.issued2008en_US
dc.identifier.citationCell Cycle, 2008, v. 7 n. 9, p. 1173-1177en_US
dc.identifier.issn1538-4101en_US
dc.identifier.urihttp://hdl.handle.net/10722/148564-
dc.description.abstractEpigenetic modifications influence gene expression pattern and provide a unique signature of a cell differentiation status. Without external stimuli or signalling events, this cell identity remains stable and unlikely to change over many cell divisions. The epigenetic signature of a particular cell fate therefore needs to be replicated faithfully in daughter cells; otherwise a cell lineage cannot be maintained. However, the mechanism of transmission of cellular memory from mother to daughter cells remains unclear. It has been suggested that the inheritance of an active or silent gene state involves different kinds of epigenetic mechanisms, e.g., DNA methylation, histone modifications, replacement of histone variants, Polycomb group (PcG) and Trithorax group (TrxG) proteins. Emerging evidence supports the role of histone variant H3.3 in maintaining an active gene status and in remodelling nucleosomal composition. Here we discuss some recent findings on the propagation of epigenetic memory and propose a model for the inheritance of an active gene state through the interaction of H3.3 with other epigenetic components. ©2008 Landes Bioscience.en_US
dc.languageengen_US
dc.publisherLandes Bioscience. The Journal's web site is located at http://www.landesbioscience.com/journals/ccen_US
dc.relation.ispartofCell Cycleen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCell Differentiation - Geneticsen_US
dc.subject.meshCell Lineage - Geneticsen_US
dc.subject.meshChromatin Assembly And Disassembly - Geneticsen_US
dc.subject.meshEpigenesis, Genetic - Geneticsen_US
dc.subject.meshGene Expression Regulation - Geneticsen_US
dc.subject.meshHistones - Geneticsen_US
dc.subject.meshHumansen_US
dc.subject.meshInheritance Patterns - Geneticsen_US
dc.subject.meshModels, Biologicalen_US
dc.subject.meshNucleosomes - Geneticsen_US
dc.titleEpigenetic inheritance of cell differentiation statusen_US
dc.typeArticleen_US
dc.identifier.emailNg, RK:rayng@pathology.hku.hken_US
dc.identifier.authorityNg, RK=rp00273en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid18418041-
dc.identifier.scopuseid_2-s2.0-44349191553en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-44349191553&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume7en_US
dc.identifier.issue9en_US
dc.identifier.spage1173en_US
dc.identifier.epage1177en_US
dc.identifier.isiWOS:000256102700010-
dc.publisher.placeUnited Statesen_US

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