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Article: Epigenetic memory of an active gene state depends on histone H3.3 incorporation into chromatin in the absence of transcription

TitleEpigenetic memory of an active gene state depends on histone H3.3 incorporation into chromatin in the absence of transcription
Authors
Issue Date2008
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/naturecellbiology
Citation
Nature Cell Biology, 2008, v. 10 n. 1, p. 102-109 How to Cite?
AbstractThe remarkable stability of gene expression in somatic cells is exemplified by the way memory of an active gene state is retained when an endoderm cell nucleus is transplanted to an enucleated egg. Here we analyse the mechanism of a similar example of epigenetic memory. We find that memory can persist through 24 cell divisions in the absence of transcription and applies to the expression of the myogenic gene MyoD in non-muscle cell lineages of nuclear transplant embryos. We show that memory is not explained by the methylation of promoter DNA. However, we demonstrate that epigenetic memory correlates with the association of histone H3.3 with the MyoD promoter in embryos that display memory but not in those where memory has been lost. The association of a mutated histone H3.3 (H3.3 E4, which lacks the methylatable H3.3 lysine 4) with promoter DNA eliminates memory, indicating a requirement of H3.3 K4 for memory. We also show that overexpression of H3.3 can enhance memory in transplanted nuclei. We therefore conclude that the association of histone H3.3 with the MyoD promoter makes a necessary contribution to this example of memory. Hence, we suggest that epigenetic memory helps to stabilize gene expression in normal development; it might also help to account for the inefficient reprogramming in some transplanted nuclei.
Persistent Identifierhttp://hdl.handle.net/10722/148536
ISSN
2015 Impact Factor: 18.699
2015 SCImago Journal Rankings: 14.131
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorNg, RKen_US
dc.contributor.authorGurdon, JBen_US
dc.date.accessioned2012-05-29T06:13:34Z-
dc.date.available2012-05-29T06:13:34Z-
dc.date.issued2008en_US
dc.identifier.citationNature Cell Biology, 2008, v. 10 n. 1, p. 102-109en_US
dc.identifier.issn1465-7392en_US
dc.identifier.urihttp://hdl.handle.net/10722/148536-
dc.description.abstractThe remarkable stability of gene expression in somatic cells is exemplified by the way memory of an active gene state is retained when an endoderm cell nucleus is transplanted to an enucleated egg. Here we analyse the mechanism of a similar example of epigenetic memory. We find that memory can persist through 24 cell divisions in the absence of transcription and applies to the expression of the myogenic gene MyoD in non-muscle cell lineages of nuclear transplant embryos. We show that memory is not explained by the methylation of promoter DNA. However, we demonstrate that epigenetic memory correlates with the association of histone H3.3 with the MyoD promoter in embryos that display memory but not in those where memory has been lost. The association of a mutated histone H3.3 (H3.3 E4, which lacks the methylatable H3.3 lysine 4) with promoter DNA eliminates memory, indicating a requirement of H3.3 K4 for memory. We also show that overexpression of H3.3 can enhance memory in transplanted nuclei. We therefore conclude that the association of histone H3.3 with the MyoD promoter makes a necessary contribution to this example of memory. Hence, we suggest that epigenetic memory helps to stabilize gene expression in normal development; it might also help to account for the inefficient reprogramming in some transplanted nuclei.en_US
dc.languageengen_US
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/naturecellbiologyen_US
dc.relation.ispartofNature Cell Biologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAzacitidine - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshBlotting, Westernen_US
dc.subject.meshChromatin - Metabolismen_US
dc.subject.meshChromatin Immunoprecipitationen_US
dc.subject.meshDna Methylation - Drug Effectsen_US
dc.subject.meshDna Modification Methylases - Antagonists & Inhibitorsen_US
dc.subject.meshEmbryo, Nonmammalian - Cytology - Embryology - Metabolismen_US
dc.subject.meshEnzyme Inhibitors - Pharmacologyen_US
dc.subject.meshEpigenesis, Geneticen_US
dc.subject.meshGene Expression Regulation, Developmentalen_US
dc.subject.meshHistones - Genetics - Metabolismen_US
dc.subject.meshModels, Biologicalen_US
dc.subject.meshMutationen_US
dc.subject.meshMyod Protein - Genetics - Metabolismen_US
dc.subject.meshNuclear Transfer Techniquesen_US
dc.subject.meshPromoter Regions, Genetic - Geneticsen_US
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_US
dc.subject.meshTranscription, Geneticen_US
dc.subject.meshXenopusen_US
dc.subject.meshXenopus Proteins - Genetics - Metabolismen_US
dc.titleEpigenetic memory of an active gene state depends on histone H3.3 incorporation into chromatin in the absence of transcriptionen_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.doi10.1038/ncb1674en_US
dc.identifier.pmid18066050-
dc.identifier.scopuseid_2-s2.0-37749051130en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-37749051130&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume10en_US
dc.identifier.issue1en_US
dc.identifier.spage102en_US
dc.identifier.epage109en_US
dc.identifier.eissn1476-4679-
dc.identifier.isiWOS:000252116100018-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.f10001097680-
dc.identifier.citeulike2090463-

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