Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/52426
DC FieldValueLanguage
dc.contributor.authorLe Bin, Gloryn Chiaen_US
dc.contributor.authorMuñoz-Descalzo, Silviaen_US
dc.contributor.authorKurowski, Agataen_US
dc.contributor.authorLeitch, Harryen_US
dc.contributor.authorLou, Xinghuaen_US
dc.contributor.authorMansfield, Williamen_US
dc.contributor.authorEtienne-Dumeau, Charlesen_US
dc.contributor.authorGrabole, Nilsen_US
dc.contributor.authorMulas, Carlaen_US
dc.contributor.authorNiwa, Hitoshien_US
dc.contributor.authorHadjantonakis, Anna Katerinaen_US
dc.contributor.authorNichols, Jenniferen_US
dc.date.accessioned2018-11-25T20:14:07Z-
dc.date.available2018-11-25T20:14:07Z-
dc.date.issued2014en_US
dc.identifier.issn0950-1991en_US
dc.identifier.urihttp://hdl.handle.net/10553/52426-
dc.description.abstractThe transcription factor Oct4 is required in vitro for establishment and maintenance of embryonic stem cells and for reprogramming somatic cells to pluripotency. In vivo, it prevents the ectopic differentiation of early embryos into trophoblast. Here, we further explore the role of Oct4 in blastocyst formation and specification of epiblast versus primitive endoderm lineages using conditional genetic deletion. Experiments involving mouse embryos deficient for both maternal and zygotic Oct4 suggest that it is dispensable for zygote formation, early cleavage and activation of Nanog expression. Nanog protein is significantly elevated in the presumptive inner cell mass of Oct4 null embryos, suggesting an unexpected role for Oct4 in attenuating the level of Nanog, which might be significant for priming differentiation during epiblast maturation. Induced deletion of Oct4 during the morula to blastocyst transition disrupts the ability of inner cell mass cells to adopt lineage-specific identity and acquire the molecular profile characteristic of either epiblast or primitive endoderm. Sox17, a marker of primitive endoderm, is not detected following prolonged culture of such embryos, but can be rescued by provision of exogenous FGF4. Interestingly, functional primitive endoderm can be rescued in Oct4-deficient embryos in embryonic stem cell complementation assays, but only if the host embryos are at the pre-blastocyst stage. We conclude that cell fate decisions within the inner cell mass are dependent upon Oct4 and that Oct4 is not cell-autonomously required for the differentiation of primitive endoderm derivatives, as long as an appropriate developmental environment is established.en_US
dc.languageengen_US
dc.relation.ispartofDevelopment (Cambridge)en_US
dc.sourceDevelopment (Cambridge)[ISSN 0950-1991],v. 141, p. 1001-1010en_US
dc.subject32 Ciencias médicasen_US
dc.subject320102 Genética clínicaen_US
dc.subject.otherBlastocysten_US
dc.subject.otherChimaeraen_US
dc.subject.otherNanogen_US
dc.subject.otherOct4 (Pou5f1)en_US
dc.subject.otherPrimitive endodermen_US
dc.subject.otherSox17en_US
dc.titleOct4 is required for lineage priming in the developing inner cell mass of the mouse blastocysten_US
dc.typeinfo:eu-repo/semantics/articleen_US
dc.typeArticleen_US
dc.identifier.doi10.1242/dev.096875en_US
dc.identifier.scopus84894067021-
dc.contributor.authorscopusid55872680700-
dc.contributor.authorscopusid9235908900-
dc.contributor.authorscopusid27368155400-
dc.contributor.authorscopusid18042063600-
dc.contributor.authorscopusid36154372500-
dc.contributor.authorscopusid26635485100-
dc.contributor.authorscopusid56037315600-
dc.contributor.authorscopusid55179392700-
dc.contributor.authorscopusid55819788000-
dc.contributor.authorscopusid56429875100-
dc.contributor.authorscopusid6701560632-
dc.contributor.authorscopusid7201486017-
dc.description.lastpage1010en_US
dc.description.firstpage1001en_US
dc.relation.volume141en_US
dc.investigacionCiencias de la Saluden_US
dc.type2Artículoen_US
dc.description.numberofpages10en_US
dc.utils.revisionen_US
dc.date.coverdateMarzo 2014en_US
dc.identifier.ulpgcen_US
dc.contributor.buulpgcBU-MEDen_US
dc.description.sjr5,204-
dc.description.jcr6,462-
dc.description.sjrqQ1-
dc.description.jcrqQ1-
dc.description.scieSCIE-
item.fulltextSin texto completo-
item.grantfulltextnone-
crisitem.author.deptGIR IUIBS: Diabetes y endocrinología aplicada-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptDepartamento de Morfología-
crisitem.author.orcid0000-0003-0939-7721-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.fullNameMuñoz Descalzo, Silvia-
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