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dc.contributor.authorCernilogar, Filippo M.
dc.contributor.authorBurroughs, A. Maxwell
dc.contributor.authorLanzuolo, Chiara
dc.contributor.authorBreiling, Achim
dc.contributor.authorImhof, Axel
dc.contributor.authorOrlando, Valerio
dc.date.accessioned2014-08-27T09:46:46Z
dc.date.available2014-08-27T09:46:46Z
dc.date.issued2013-06-13
dc.identifier.citationCernilogar FM, Burroughs AM, Lanzuolo C, Breiling A, Imhof A, et al. (2013) RNA-Interference Components Are Dispensable for Transcriptional Silencing of the Drosophila Bithorax-Complex. PLoS ONE 8: e65740. doi:10.1371/journal.pone.0065740.
dc.identifier.issn19326203
dc.identifier.pmid23785447
dc.identifier.doi10.1371/journal.pone.0065740
dc.identifier.urihttp://hdl.handle.net/10754/325319
dc.description.abstractBackground:Beyond their role in post-transcriptional gene silencing, Dicer and Argonaute, two components of the RNA interference (RNAi) machinery, were shown to be involved in epigenetic regulation of centromeric heterochromatin and transcriptional gene silencing. In particular, RNAi mechanisms appear to play a role in repeat induced silencing and some aspects of Polycomb-mediated gene silencing. However, the functional interplay of RNAi mechanisms and Polycomb group (PcG) pathways at endogenous loci remains to be elucidated.Principal Findings:Here we show that the endogenous Dicer-2/Argonaute-2 RNAi pathway is dispensable for the PcG mediated silencing of the homeotic Bithorax Complex (BX-C). Although Dicer-2 depletion triggers mild transcriptional activation at Polycomb Response Elements (PREs), this does not induce transcriptional changes at PcG-repressed genes. Moreover, Dicer-2 is not needed to maintain global levels of methylation of lysine 27 of histone H3 and does not affect PRE-mediated higher order chromatin structures within the BX-C. Finally bioinformatic analysis, comparing published data sets of PcG targets with Argonaute-2-bound small RNAs reveals no enrichment of these small RNAs at promoter regions associated with PcG proteins.Conclusions:We conclude that the Dicer-2/Argonaute-2 RNAi pathway, despite its role in pairing sensitive gene silencing of transgenes, does not have a role in PcG dependent silencing of major homeotic gene cluster loci in Drosophila. © 2013 Cernilogar et al.
dc.language.isoen
dc.publisherPublic Library of Science (PLoS)
dc.rightsThis is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
dc.rightsArchived with thanks to PLoS ONE
dc.subjectargonaute 2 protein
dc.subjectbithorax complex
dc.subjectdicer
dc.subjectDNA
dc.subjecthistone H3
dc.subjectlysine
dc.subjectpolycomb group protein
dc.subjectsmall interfering RNA
dc.subjectunclassified drug
dc.subjectanimal cell
dc.subjectbioinformatics
dc.subjectchromatin structure
dc.subjectcontrolled study
dc.subjectDNA responsive element
dc.subjectDrosophila
dc.subjectgene cluster
dc.subjectgene locus
dc.subjectgene repression
dc.subjectgene silencing
dc.subjecthistone methylation
dc.subjectpromoter region
dc.subjectprotein depletion
dc.subjectRNA interference
dc.subjecttranscription initiation
dc.subjecttransgene
dc.subjectArgonaute Proteins
dc.subjectDrosophila
dc.subjectDrosophila Proteins
dc.subjectGene Silencing
dc.subjectHistones
dc.subjectMethylation
dc.subjectPolycomb-Group Proteins
dc.subjectResponse Elements
dc.subjectRibonuclease III
dc.subjectRNA Helicases
dc.subjectRNA Interference
dc.subjectRNA, Double-Stranded
dc.subjectTranscription, Genetic
dc.titleRNA-Interference Components Are Dispensable for Transcriptional Silencing of the Drosophila Bithorax-Complex
dc.typeArticle
dc.contributor.departmentBiological and Environmental Sciences and Engineering (BESE) Division
dc.contributor.departmentBioscience Program
dc.contributor.departmentKAUST Environmental Epigenetics Research Program (KEEP)
dc.identifier.journalPLoS ONE
dc.identifier.pmcidPMC3681981
dc.eprint.versionPublisher's Version/PDF
dc.contributor.institutionEpigenetics and Genome Reprogramming Laboratory, IRCCS Fondazione Santa Lucia, Rome, Italy
dc.contributor.institutionAdolf-Butenandt Institute, Ludwig Maximilian University of Munich, Munich, Germany
dc.contributor.institutionDivision of Epigenetics, DKFZ-ZMBH Alliance, German Cancer Research Center, Heidelberg, Germany
dc.contributor.institutionCNR Institute of Neurobiology and Molecular Medicine, IRCCS Santa Lucia Foundation, Rome, Italy
dc.contributor.institutionRIKEN Omics Science Center, RIKEN Yokohama Institute, Tsurumi-ku, Yokohama, Kanagawa, Japan
dc.contributor.institutionMunich Center of Integrated Protein Science, Ludwig Maximilian University of Munich, Munich, Germany
dc.contributor.institutionNational Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Bethesda, MD, United States
dc.contributor.affiliationKing Abdullah University of Science and Technology (KAUST)
kaust.personOrlando, Valerio
refterms.dateFOA2018-06-13T14:59:08Z


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