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dc.contributor.authorMagklara, Angeliki
dc.contributor.authorYen, Angela
dc.contributor.authorColquitt, Bradley M.
dc.contributor.authorClowney, E. Josephine
dc.contributor.authorAllen, William
dc.contributor.authorMarkenscoff-Papadimitriou, Eirene
dc.contributor.authorEvans, Zoe A.
dc.contributor.authorKheradpour, Pouya
dc.contributor.authorMountoufaris, George
dc.contributor.authorCarey, Catriona
dc.contributor.authorBarnea, Gilad
dc.contributor.authorKellis, Manolis
dc.contributor.authorLomvardas, Stavros
dc.date.accessioned2014-05-22T18:56:02Z
dc.date.available2014-05-22T18:56:02Z
dc.date.issued2011-05
dc.date.submitted2011-03
dc.identifier.issn00928674
dc.identifier.urihttp://hdl.handle.net/1721.1/87107
dc.description.abstractConstitutive heterochromatin is traditionally viewed as the static form of heterochromatin that silences pericentromeric and telomeric repeats in a cell cycle- and differentiation-independent manner. Here, we show that, in the mouse olfactory epithelium, olfactory receptor (OR) genes are marked in a highly dynamic fashion with the molecular hallmarks of constitutive heterochromatin, H3K9me3 and H4K20me3. The cell type and developmentally dependent deposition of these marks along the OR clusters are, most likely, reversed during the process of OR choice to allow for monogenic and monoallelic OR expression. In contrast to the current view of OR choice, our data suggest that OR silencing takes place before OR expression, indicating that it is not the product of an OR-elicited feedback signal. Our findings suggest that chromatin-mediated silencing lays a molecular foundation upon which singular and stochastic selection for gene expression can be applied.en_US
dc.description.sponsorshipNational Science Foundation (U.S.) (Fellowship)en_US
dc.description.sponsorshipBrown University (Royce Fellowship)en_US
dc.description.sponsorshipPew Charitable Trusts (Pew Scholar of the Biomedical Sciences)en_US
dc.description.sponsorshipMcKnight Endowment Fund for Neuroscienceen_US
dc.description.sponsorshipRett Syndrome Research Trusten_US
dc.description.sponsorshipHellman Family Foundationen_US
dc.description.sponsorshipNational Institute on Deafness and Other Communication Disorders (U.S.) (R03 DC010273)en_US
dc.description.sponsorshipNational Institutes of Health (U.S.) (Director’s New Innovator Award Program (1DPOD006667))en_US
dc.language.isoen_US
dc.publisherElsevier B.V.en_US
dc.relation.isversionofhttp://dx.doi.org/10.1016/j.cell.2011.03.040en_US
dc.rightsArticle is made available in accordance with the publisher's policy and may be subject to US copyright law. Please refer to the publisher's site for terms of use.en_US
dc.sourceElsevier Open Archiveen_US
dc.titleAn Epigenetic Signature for Monoallelic Olfactory Receptor Expressionen_US
dc.typeArticleen_US
dc.identifier.citationMagklara, Angeliki, Angela Yen, Bradley M. Colquitt, E. Josephine Clowney, William Allen, Eirene Markenscoff-Papadimitriou, Zoe A. Evans, et al. “An Epigenetic Signature for Monoallelic Olfactory Receptor Expression.” Cell 145, no. 4 (May 2011): 555–570. © 2011 Elsevier.en_US
dc.contributor.departmentMassachusetts Institute of Technology. Computer Science and Artificial Intelligence Laboratoryen_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Electrical Engineering and Computer Scienceen_US
dc.contributor.mitauthorYen, Angelaen_US
dc.contributor.mitauthorKheradpour, Pouyaen_US
dc.contributor.mitauthorKellis, Manolisen_US
dc.relation.journalCellen_US
dc.eprint.versionFinal published versionen_US
dc.type.urihttp://purl.org/eprint/type/JournalArticleen_US
eprint.statushttp://purl.org/eprint/status/PeerRevieweden_US
dspace.orderedauthorsMagklara, Angeliki; Yen, Angela; Colquitt, Bradley M.; Clowney, E. Josephine; Allen, William; Markenscoff-Papadimitriou, Eirene; Evans, Zoe A.; Kheradpour, Pouya; Mountoufaris, George; Carey, Catriona; Barnea, Gilad; Kellis, Manolis; Lomvardas, Stavrosen_US
dc.identifier.orcidhttps://orcid.org/0000-0001-5951-9358
mit.licensePUBLISHER_POLICYen_US
mit.metadata.statusComplete


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