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dc.creatorGómez Zambrano, Ángeleses
dc.creatorMerini, Wiames
dc.creatorCalonje Macaya, Miriames
dc.date.accessioned2020-10-21T14:01:56Z
dc.date.available2020-10-21T14:01:56Z
dc.date.issued2019
dc.identifier.citationGómez Zambrano, Á., Merini, W. y Calonje Macaya, M. (2019). The repressive role of Arabidopsis H2A.Z in transcriptional regulation depends on AtBMI1 activity. Nature Communications, 10 (1), 2828-.
dc.identifier.issn2041-1723es
dc.identifier.urihttps://hdl.handle.net/11441/102115
dc.description.abstractH2A.Z variant has emerged as a critical player in regulating plant responses to environment; however, the mechanism by which H2A.Z mediates this regulation remains unclear. In Arabidopsis, H2A.Z has been proposed to have opposite effects on transcription depending on its localization within the gene. These opposite roles have been assigned by correlating gene expression and H2A.Z enrichment analyses but without considering the impact of possible H2A.Z post-translational modifications. Here, we show that H2A.Z can be monoubiquitinated by the PRC1 components AtBMI1A/B/C. The incorporation of this modification is required for H2A.Z-mediated transcriptional repression through a mechanism that does not require PRC2 activity. Our data suggest that the dual role of H2A.Z in regulating gene expression depends on the modification that it carries, while the levels of H2A.Z within genes depend on the transcriptional activity.es
dc.formatapplication/pdfes
dc.format.extent12 p.es
dc.language.isoenges
dc.publisherSpringer Naturees
dc.relation.ispartofNature Communications, 10 (1), 2828-.
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.titleThe repressive role of Arabidopsis H2A.Z in transcriptional regulation depends on AtBMI1 activityes
dc.typeinfo:eu-repo/semantics/articlees
dcterms.identifierhttps://ror.org/03yxnpp24
dc.type.versioninfo:eu-repo/semantics/publishedVersiones
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses
dc.relation.publisherversionhttp://dx.doi.org/10.1038/s41467-019-10773-1es
dc.identifier.doi10.1038/s41467-019-10773-1es
dc.journaltitleNature Communicationses
dc.publication.volumen10es
dc.publication.issue1es
dc.publication.initialPage2828es

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