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dc.contributor.authorNarendra, Varun
dc.contributor.authorBulajic, Milica
dc.contributor.authorDekker, Job
dc.contributor.authorMazzoni, Esteban O.
dc.contributor.authorReinberg, Danny
dc.date2022-08-11T08:11:00.000
dc.date.accessioned2022-08-23T17:27:56Z
dc.date.available2022-08-23T17:27:56Z
dc.date.issued2016-12-15
dc.date.submitted2017-01-20
dc.identifier.citationGenes Dev. 2016 Dec 15;30(24):2657-2662. doi: 10.1101/gad.288324.116. <a href="http://dx.doi.org/10.1101/gad.288324.116">Link to article on publisher's site</a>.
dc.identifier.issn0890-9369 (Linking)
dc.identifier.doi10.1101/gad.288324.116
dc.identifier.pmid28087711
dc.identifier.urihttp://hdl.handle.net/20.500.14038/49973
dc.description.abstractThe genome is organized into repeating topologically associated domains (TADs), each of which is spatially isolated from its neighbor by poorly understood boundary elements thought to be conserved across cell types. Here, we show that deletion of CTCF (CCCTC-binding factor)-binding sites at TAD and sub-TAD topological boundaries that form within the HoxA and HoxC clusters during differentiation not only disturbs local chromatin domain organization and regulatory interactions but also results in homeotic transformations typical of Hox gene misregulation. Moreover, our data suggest that CTCF-dependent boundary function can be modulated by competing forces, such as the self-assembly of polycomb domains within the nucleus. Therefore, CTCF boundaries are not merely static structural components of the genome but instead are locally dynamic regulatory structures that control gene expression during development.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=28087711&dopt=Abstract">Link to Article in PubMed</a>
dc.rights© 2016 Narendra et al. This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.
dc.rights.urihttp://creativecommons.org/licenses/by-nc/4.0/
dc.subjectCTCF
dc.subjectHox gene regulation
dc.subjectPolycomb/Trithorax
dc.subjectTADs
dc.subjectchromatin and epigenetics
dc.subjectchromosomal conformation
dc.subjectBiochemistry
dc.subjectComputational Biology
dc.subjectDevelopmental Biology
dc.subjectGenomics
dc.subjectMolecular Biology
dc.subjectStructural Biology
dc.subjectSystems Biology
dc.titleCTCF-mediated topological boundaries during development foster appropriate gene regulation
dc.typeJournal Article
dc.source.journaltitleGenes and development
dc.source.volume30
dc.source.issue24
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=1094&amp;context=sysbio_pubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/sysbio_pubs/95
dc.legacy.embargo2017-06-15T00:00:00-07:00
dc.identifier.contextkey9563182
refterms.dateFOA2022-08-23T17:27:56Z
html.description.abstract<p>The genome is organized into repeating topologically associated domains (TADs), each of which is spatially isolated from its neighbor by poorly understood boundary elements thought to be conserved across cell types. Here, we show that deletion of CTCF (CCCTC-binding factor)-binding sites at TAD and sub-TAD topological boundaries that form within the HoxA and HoxC clusters during differentiation not only disturbs local chromatin domain organization and regulatory interactions but also results in homeotic transformations typical of Hox gene misregulation. Moreover, our data suggest that CTCF-dependent boundary function can be modulated by competing forces, such as the self-assembly of polycomb domains within the nucleus. Therefore, CTCF boundaries are not merely static structural components of the genome but instead are locally dynamic regulatory structures that control gene expression during development.</p>
dc.identifier.submissionpathsysbio_pubs/95
dc.contributor.departmentDepartment of Biochemistry and Molecular Pharmacology
dc.contributor.departmentProgram in Systems Biology
dc.source.pages2657-2662


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© 2016 Narendra et al. This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.
Except where otherwise noted, this item's license is described as © 2016 Narendra et al. This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.