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dc.contributor.authorHardy, Sara
dc.contributor.authorJacques, Pierre-Étienne
dc.contributor.authorGévry, Nicolas
dc.contributor.authorForest, Audrey
dc.contributor.authorFortin, Marie-Ève
dc.contributor.authorLaflamme, Liette
dc.contributor.authorGaudreau, Luc
dc.contributor.authorRobert, François
dc.date.accessioned2009-11-22T16:43:14Z
dc.date.available2009-11-22T16:43:14Z
dc.date.issued2009
dc.identifier.urihttp://hdl.handle.net/1866/3171
dc.description.sponsorshipThis work was supported by a grant from the Canadian Cancer Society to LG and FR. FR was a New Investigator Award from the CIHR and is now a Chercheur boursier (junior 2) from the FRSQ, LG holds a Canada research chair on mechanisms of gene transcription, and NG was a recipient of a post-doctoral fellowship from NSERC. PEJ and SH both hold post-doctoral awards from the IRCM training program in cancer research funded by the CIHR.en
dc.titleThe euchromatic and heterochromatic landscapes are shaped by antagonizing effects of transcription on H2A.Z depositionen
dc.typeArticleen
dc.contributor.affiliationUniversité de Montréal. Faculté de médecine. Institut de recherches cliniques de Montréalfr
dc.contributor.affiliationUniversité de Montréal. Faculté de médecine. Département de médecinefr
dc.identifier.doi10.1371/journal.pgen.1000687
dcterms.abstractA role for variant histone H2A.Z in gene expression is now well established but little is known about the mechanisms by which it operates. Using a combination of ChIP-chip, knockdown and expression profiling experiments, we show that upon gene induction, human H2A.Z associates with gene promoters and helps in recruiting the transcriptional machinery. Surprisingly, we also found that H2A.Z is randomly incorporated in the genome at low levels and that active transcription antagonizes this incorporation in transcribed regions. After cessation of transcription, random H2A.Z quickly reappears on genes, demonstrating that this incorporation utilizes an active mechanism. Within facultative heterochromatin, we observe a hyper accumulation of the variant histone, which might be due to the lack of transcription in these regions. These results show how chromatin structure and transcription can antagonize each other, therefore shaping chromatin and controlling gene expression.en
dcterms.languageengen
UdeM.VersionRioxxVersion acceptée / Accepted Manuscript
oaire.citationTitlePLoS genetics
oaire.citationVolume5
oaire.citationIssue10


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