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dc.contributor.authorKim, Heesun
dc.contributor.authorDing, Yue-He
dc.contributor.authorZhang, Gangming
dc.contributor.authorYan, Yong-Hong
dc.contributor.authorConte, Darryl Jr.
dc.contributor.authorDong, Meng-Qiu
dc.contributor.authorMello, Craig C.
dc.date2022-08-11T08:10:00.000
dc.date.accessioned2022-08-23T16:51:45Z
dc.date.available2022-08-23T16:51:45Z
dc.date.issued2021-05-18
dc.date.submitted2021-09-02
dc.identifier.citation<p>Kim H, Ding YH, Zhang G, Yan YH, Conte D Jr, Dong MQ, Mello CC. HDAC1 SUMOylation promotes Argonaute-directed transcriptional silencing in <em>C. elegans</em>. Elife. 2021 May 18;10:e63299. doi: 10.7554/eLife.63299. PMID: 34003109; PMCID: PMC8131101. <a href="https://doi.org/10.7554/eLife.63299">Link to article on publisher's site</a></p>
dc.identifier.issn2050-084X (Linking)
dc.identifier.doi10.7554/eLife.63299
dc.identifier.pmid34003109
dc.identifier.urihttp://hdl.handle.net/20.500.14038/41918
dc.description.abstractEukaryotic cells use guided search to coordinately control dispersed genetic elements. Argonaute proteins and their small RNA cofactors engage nascent RNAs and chromatin-associated proteins to direct transcriptional silencing. The small ubiquitin-like modifier (SUMO) has been shown to promote the formation and maintenance of silent chromatin (called heterochromatin) in yeast, plants, and animals. Here, we show that Argonaute-directed transcriptional silencing in Caenorhabditis elegans requires SUMOylation of the type 1 histone deacetylase HDA-1. Our findings suggest how SUMOylation promotes the association of HDAC1 with chromatin remodeling factors and with a nuclear Argonaute to initiate de novo heterochromatin silencing.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=34003109&dopt=Abstract">Link to Article in PubMed</a></p>
dc.rightsCopyright © 2021, Kim et al. This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectC. elegans
dc.subjectHDAC SUMOylation
dc.subjectdevelopmental biology
dc.subjectgermline
dc.subjectnuclear argonaut
dc.subjectAmino Acids, Peptides, and Proteins
dc.subjectDevelopmental Biology
dc.titleHDAC1 SUMOylation promotes Argonaute-directed transcriptional silencing in C. elegans
dc.typeJournal Article
dc.source.journaltitleeLife
dc.source.volume10
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=5757&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/4724
dc.identifier.contextkey24636124
refterms.dateFOA2022-08-23T16:51:45Z
html.description.abstract<p>Eukaryotic cells use guided search to coordinately control dispersed genetic elements. Argonaute proteins and their small RNA cofactors engage nascent RNAs and chromatin-associated proteins to direct transcriptional silencing. The small ubiquitin-like modifier (SUMO) has been shown to promote the formation and maintenance of silent chromatin (called heterochromatin) in yeast, plants, and animals. Here, we show that Argonaute-directed transcriptional silencing in Caenorhabditis elegans requires SUMOylation of the type 1 histone deacetylase HDA-1. Our findings suggest how SUMOylation promotes the association of HDAC1 with chromatin remodeling factors and with a nuclear Argonaute to initiate de novo heterochromatin silencing.</p>
dc.identifier.submissionpathoapubs/4724
dc.contributor.departmentRNA Therapeutics Institute
dc.source.pagese63299


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Copyright © 2021, Kim et al. This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.
Except where otherwise noted, this item's license is described as Copyright © 2021, Kim et al. This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.