Please use this identifier to cite or link to this item: https://doi.org/10.1038/srep08007
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dc.titleEmbryonic stem cell differentiation requires full length Chd1
dc.contributor.authorPiatti, P
dc.contributor.authorLim, C.Y
dc.contributor.authorNat, R
dc.contributor.authorVillunger, A
dc.contributor.authorGeley, S
dc.contributor.authorShue, Y.T
dc.contributor.authorSoratroi, C
dc.contributor.authorMoser, M
dc.contributor.authorLusser, A
dc.date.accessioned2020-10-20T03:16:38Z
dc.date.available2020-10-20T03:16:38Z
dc.date.issued2015
dc.identifier.citationPiatti, P, Lim, C.Y, Nat, R, Villunger, A, Geley, S, Shue, Y.T, Soratroi, C, Moser, M, Lusser, A (2015). Embryonic stem cell differentiation requires full length Chd1. Scientific Reports 5 : 8007. ScholarBank@NUS Repository. https://doi.org/10.1038/srep08007
dc.identifier.issn20452322
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/177764
dc.description.abstractThe modulation of chromatin dynamics by ATP-dependent chromatin remodeling factors has been recognized as an important mechanism to regulate the balancing of self-renewal and pluripotency in embryonic stem cells (ESCs). Here we have studied the effects of a partial deletion of the gene encoding the chromatin remodeling factor Chd1 that generates an N-terminally truncated version of Chd1 in mouse ESCs in vitro as well as in vivo. We found that a previously uncharacterized serine-rich region (SRR) at the N-terminus is not required for chromatin assembly activity of Chd1 but that it is subject to phosphorylation. Expression of Chd1 lacking this region in ESCs resulted in aberrant differentiation properties of these cells. The self-renewal capacity and ESC chromatin structure, however, were not affected. Notably, we found that newly established ESCs derived from Chd1?2/?2 mutant mice exhibited similar differentiation defects as in vitro generated mutant ESCs, even though the N-terminal truncation of Chd1 was fully compatible with embryogenesis and post-natal life in the mouse. These results underscore the importance of Chd1 for the regulation of pluripotency in ESCs and provide evidence for a hitherto unrecognized critical role of the phosphorylated N-terminal SRR for full functionality of Chd1.
dc.publisherNature Publishing Group
dc.rightsAttribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.sourceUnpaywall 20201031
dc.subjectChd1 protein, mouse
dc.subjectDNA binding protein
dc.subjectserine
dc.subjectanimal
dc.subjectbiosynthesis
dc.subjectcell differentiation
dc.subjectchromatin assembly and disassembly
dc.subjectembryo development
dc.subjectembryonic stem cell
dc.subjectgene expression regulation
dc.subjectgenetics
dc.subjectmouse
dc.subjectAnimals
dc.subjectCell Differentiation
dc.subjectChromatin Assembly and Disassembly
dc.subjectDNA-Binding Proteins
dc.subjectEmbryonic Development
dc.subjectEmbryonic Stem Cells
dc.subjectGene Expression Regulation, Developmental
dc.subjectMice
dc.subjectSerine
dc.typeArticle
dc.contributor.departmentDEPT OF BIOCHEMISTRY
dc.description.doi10.1038/srep08007
dc.description.sourcetitleScientific Reports
dc.description.volume5
dc.description.page8007
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