Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-7376
Authors: Bräutigam, Christien
Raggioli, Angelo
Winter, Jennifer
Title: The Wnt/beta-catenin pathway regulates the expression of the miR-302 cluster in mouse ESCs and P19 cells
Online publication date: 12-Jul-2022
Language: english
Abstract: MicroRNAs of the miR-302 cluster are involved in early embryonic development and somatic cell reprogramming. Expression of the miR-302 gene is regulated by the binding of the pluripotency factors Oct4, Sox2 and Nanog to the miR-302 promoter. The specific expression pattern of the miR-302 gene suggested that additional transcription factors might be involved in its regulation. Here, we show that the miR-302 promoter is a direct target of the Wnt/beta-catenin signaling pathway. We found that the miR-302 promoter contains three different functional Tcf/Lef binding sites. Two of the three sites were located within the cluster of Oct4/Sox2/Nanog binding sites and were essential for Wnt/beta-catenin-mediated regulation of the miR-302 gene. Tcf3, the only Tcf/Lef factor that bound to the miR-302 promoter, acted as a repressor of miR-302 transcription. Interestingly, mutations in the two Tcf/Lef binding sites and the Oct4/Nanog binding sites abolished miR-302 promoter responsiveness to Wnt signaling, suggesting that the Tcf/Lef and the Oct4/Nanog sites interact genetically.
DDC: 610 Medizin
610 Medical sciences
Institution: Johannes Gutenberg-Universität Mainz
Department: FB 04 Medizin
Place: Mainz
ROR: https://ror.org/023b0x485
DOI: http://doi.org/10.25358/openscience-7376
Version: Published version
Publication type: Zeitschriftenaufsatz
License: CC BY
Information on rights of use: https://creativecommons.org/licenses/by/3.0/
Journal: PLoS one
8
9
Pages or article number: e75315
Publisher: PLoS
Publisher place: Lawrence, Kan.
Issue date: 2013
ISSN: 1932-6203
Publisher URL: http://dx.doi.org/10.1371/journal.pone.0075315
Publisher DOI: 10.1371/journal.pone.0075315
Appears in collections:DFG-OA-Publizieren (2012 - 2017)

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