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Article: Xist Intron 1 Repression by Transcriptional-Activator-Like Effectors Designer Transcriptional Factor Improves Somatic Cell Reprogramming in Mice

TitleXist Intron 1 Repression by Transcriptional-Activator-Like Effectors Designer Transcriptional Factor Improves Somatic Cell Reprogramming in Mice
Authors
Keywordsembryo
enhancer region
epigenetics
female
gene
Issue Date2019
PublisherAlphaMed Press. The Journal's web site is located at http://www.stemcells.com
Citation
Stem Cells, 2019, v. 37 n. 5, p. 599-608 How to Cite?
AbstractXist is the master regulator of X chromosome inactivation. In order to further understand the Xist locus in the reprogramming of somatic cells to induced pluripotent stem cells (iPSCs) and in somatic cell nuclear transfer (SCNT), we tested transcription‐activator‐like effectors‐based designer transcriptional factors (dTFs), which were specific to numerous regions at the Xist locus. We report that the selected dTF repressor 6 (R6) binding the intron 1 of Xist, which caused higher H3K9me3 followed by X chromosome opening and repression of X‐linked genes in mouse embryonic fibroblasts, rather than affecting Xist expression, substantially improved the iPSC generation and the SCNT preimplantation embryo development. Conversely, the dTF activator targeting the same genomic region of R6 decreased iPSC formation and blocked SCNT‐embryo development. These results thus uncover the critical requirement for the Xist locus in epigenetic resetting, which is not directly related to Xist transcription. This may provide a unique route to improving the reprogramming. Stem Cells 2019;37:599–608
DescriptionLink to Free access
Persistent Identifierhttp://hdl.handle.net/10722/290510
ISSN
2019 Impact Factor: 6.022
2015 SCImago Journal Rankings: 3.438
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorZhang, J-
dc.contributor.authorGao, X-
dc.contributor.authorYang, J-
dc.contributor.authorFan, X-
dc.contributor.authorWang, W-
dc.contributor.authorLiang, Y-
dc.contributor.authorFan, L-
dc.contributor.authorHan, H-
dc.contributor.authorXu, X-
dc.contributor.authorTang, F-
dc.contributor.authorBao, S-
dc.contributor.authorLiu, P-
dc.contributor.authorLi, X-
dc.date.accessioned2020-11-02T05:43:16Z-
dc.date.available2020-11-02T05:43:16Z-
dc.date.issued2019-
dc.identifier.citationStem Cells, 2019, v. 37 n. 5, p. 599-608-
dc.identifier.issn1066-5099-
dc.identifier.urihttp://hdl.handle.net/10722/290510-
dc.descriptionLink to Free access-
dc.description.abstractXist is the master regulator of X chromosome inactivation. In order to further understand the Xist locus in the reprogramming of somatic cells to induced pluripotent stem cells (iPSCs) and in somatic cell nuclear transfer (SCNT), we tested transcription‐activator‐like effectors‐based designer transcriptional factors (dTFs), which were specific to numerous regions at the Xist locus. We report that the selected dTF repressor 6 (R6) binding the intron 1 of Xist, which caused higher H3K9me3 followed by X chromosome opening and repression of X‐linked genes in mouse embryonic fibroblasts, rather than affecting Xist expression, substantially improved the iPSC generation and the SCNT preimplantation embryo development. Conversely, the dTF activator targeting the same genomic region of R6 decreased iPSC formation and blocked SCNT‐embryo development. These results thus uncover the critical requirement for the Xist locus in epigenetic resetting, which is not directly related to Xist transcription. This may provide a unique route to improving the reprogramming. Stem Cells 2019;37:599–608-
dc.languageeng-
dc.publisherAlphaMed Press. The Journal's web site is located at http://www.stemcells.com-
dc.relation.ispartofStem Cells-
dc.subjectembryo-
dc.subjectenhancer region-
dc.subjectepigenetics-
dc.subjectfemale-
dc.subjectgene-
dc.titleXist Intron 1 Repression by Transcriptional-Activator-Like Effectors Designer Transcriptional Factor Improves Somatic Cell Reprogramming in Mice-
dc.typeArticle-
dc.identifier.emailLiu, P: pliu88@hku.hk-
dc.identifier.authorityLiu, P=rp02328-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/stem.2928-
dc.identifier.pmid30353613-
dc.identifier.scopuseid_2-s2.0-85065034571-
dc.identifier.hkuros317867-
dc.identifier.volume37-
dc.identifier.issue5-
dc.identifier.spage599-
dc.identifier.epage608-
dc.identifier.isiWOS:000466952000008-
dc.publisher.placeUnited States-
dc.identifier.issnl1066-5099-

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