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dc.contributor.authorJachowicz, Joanna W.
dc.contributor.authorBing, Xin Y.
dc.contributor.authorPontabry, Julien
dc.contributor.authorBoskovic, Ana
dc.contributor.authorRando, Oliver J.
dc.contributor.authorTorres-Padilla, Maria-Elena
dc.date2022-08-11T08:09:20.000
dc.date.accessioned2022-08-23T16:26:49Z
dc.date.available2022-08-23T16:26:49Z
dc.date.issued2017-10-01
dc.date.submitted2017-12-22
dc.identifier.citationNat Genet. 2017 Oct;49(10):1502-1510. doi: 10.1038/ng.3945. Epub 2017 Aug 28. <a href="https://doi.org/10.1038/ng.3945">Link to article on publisher's site</a>
dc.identifier.issn1061-4036 (Linking)
dc.identifier.doi10.1038/ng.3945
dc.identifier.pmid28846101
dc.identifier.urihttp://hdl.handle.net/20.500.14038/36643
dc.description.abstractAfter fertilization, to initiate development, gametes are reprogramed to become totipotent. Approximately half of the mammalian genome consists of repetitive elements, including retrotransposons, some of which are transcribed after fertilization. Retrotransposon activation is generally assumed to be a side effect of the extensive chromatin remodeling underlying the epigenetic reprogramming of gametes. Here, we used a targeted epigenomic approach to address whether specific retrotransposon families play a direct role in chromatin organization and developmental progression. We demonstrate that premature silencing of LINE-1 elements decreases chromatin accessibility, whereas prolonged activation prevents the gradual chromatin compaction that occurs naturally in developmental progression. Preventing LINE-1 activation and interfering with its silencing decreases developmental rates independently of the coding nature of the LINE-1 transcript, thus suggesting that LINE-1 functions primarily at the chromatin level. Our data suggest that activation of LINE-1 regulates global chromatin accessibility at the beginning of development and indicate that retrotransposon activation is integral to the developmental program.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=28846101&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttps://doi.org/10.1038/ng.3945
dc.subjectBiochemistry
dc.subjectCell Biology
dc.subjectCellular and Molecular Physiology
dc.subjectDevelopmental Biology
dc.subjectGenomics
dc.subjectMolecular Biology
dc.titleLINE-1 activation after fertilization regulates global chromatin accessibility in the early mouse embryo
dc.typeJournal Article
dc.source.journaltitleNature genetics
dc.source.volume49
dc.source.issue10
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/metnet_pubs/163
dc.identifier.contextkey11293385
html.description.abstract<p>After fertilization, to initiate development, gametes are reprogramed to become totipotent. Approximately half of the mammalian genome consists of repetitive elements, including retrotransposons, some of which are transcribed after fertilization. Retrotransposon activation is generally assumed to be a side effect of the extensive chromatin remodeling underlying the epigenetic reprogramming of gametes. Here, we used a targeted epigenomic approach to address whether specific retrotransposon families play a direct role in chromatin organization and developmental progression. We demonstrate that premature silencing of LINE-1 elements decreases chromatin accessibility, whereas prolonged activation prevents the gradual chromatin compaction that occurs naturally in developmental progression. Preventing LINE-1 activation and interfering with its silencing decreases developmental rates independently of the coding nature of the LINE-1 transcript, thus suggesting that LINE-1 functions primarily at the chromatin level. Our data suggest that activation of LINE-1 regulates global chromatin accessibility at the beginning of development and indicate that retrotransposon activation is integral to the developmental program.</p>
dc.identifier.submissionpathmetnet_pubs/163
dc.contributor.departmentUMass Metabolic Network
dc.contributor.departmentDepartment of Biochemistry and Molecular Pharmacology
dc.source.pages1502-1510


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