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The BAF and PRC2 Complex Subunits Dpf2 and Eed Antagonistically Converge on Tbx3 to Control ESC Differentiation
Soochow Univ, Cam Su Genom Resource Ctr, Suzhou 215123, Peoples R China.;Wellcome Sanger Inst, Hinxton CB10 1SA, England..
Univ Calif Los Angeles, David Geffen Sch Med, Dept Biol & Chem, Los Angeles, CA 90095 USA.;Univ Calif Los Angeles, Eli & Edythe Broad Ctr Regenerat Med & Stem Cell, Los Angeles, CA USA.;Univ Calif Los Angeles, Jonsson Comprehens Canc Ctr, Bioinformat Program, Los Angeles, CA 90024 USA.;Univ Calif Los Angeles, Mol Biol Inst, Los Angeles, CA 90095 USA..
Wellcome Sanger Inst, Hinxton CB10 1SA, England..
Soochow Univ, Cam Su Genom Resource Ctr, Suzhou 215123, Peoples R China..
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2019 (English)In: Cell Stem Cell, ISSN 1934-5909, E-ISSN 1875-9777, Vol. 24, no 1, p. 138-+Article in journal (Refereed) Published
Abstract [en]

BAF complexes are composed of different subunits with varying functional and developmental roles, although many subunits have not been examined in depth. Here we show that the Baf45 subunit Dpf2 maintains pluripotency and ESC differentiation potential. Dpf2 co-occupies enhancers with Oct4, Sox2, p300, and the BAF subunit Brg1, and deleting Dpf2 perturbs ESC self-renewal, induces repression of Tbx3, and impairs mesendodermal differentiation without dramatically altering Brg1 localization. Mesendodermal differentiation can be rescued by restoring Tbx3 expression, whose distal enhancer is positively regulated by Dpf2-dependent H3K27ac maintenance and recruitment of pluripotency TFs and Brg1. In contrast, the PRC2 subunit Eed binds an intragenic Tbx3 enhancer to oppose Dpf2-dependent Tbx3 expression and mesendodermal differentiation. The PRC2 subunit Ezh2 likewise opposes Dpf2-dependent differentiation through a distinct mechanism involving Nanog repression. Together, these findings delineate distinct mechanistic roles for specific BAF and PRC2 subunits during ESC differentiation.

Place, publisher, year, edition, pages
CELL PRESS , 2019. Vol. 24, no 1, p. 138-+
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Developmental Biology
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URN: urn:nbn:se:kth:diva-241316DOI: 10.1016/j.stem.2018.12.001ISI: 000454836900015PubMedID: 30609396Scopus ID: 2-s2.0-85058662637OAI: oai:DiVA.org:kth-241316DiVA, id: diva2:1282561
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QC 20190125

Available from: 2019-01-25 Created: 2019-01-25 Last updated: 2019-01-25Bibliographically approved

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Spalinskas, RapolasSahlén, Pelin

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