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The evolutionally-conserved function of group B1 Sox family members confers the unique role of Sox2 in mouse ES cells

BACKGROUND: In mouse ES cells, the function of Sox2 is essential for the maintenance of pluripotency. Since the Sox-family of transcription factors are well conserved in the animal kingdom, addressing the evolutionary origin of Sox2 function in pluripotent stem cells is intriguing from the perspecti...

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Autores principales: Niwa, Hitoshi, Nakamura, Akira, Urata, Makoto, Shirae-Kurabayashi, Maki, Kuraku, Shigehiro, Russell, Steven, Ohtsuka, Satoshi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5007870/
https://www.ncbi.nlm.nih.gov/pubmed/27582319
http://dx.doi.org/10.1186/s12862-016-0755-4
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author Niwa, Hitoshi
Nakamura, Akira
Urata, Makoto
Shirae-Kurabayashi, Maki
Kuraku, Shigehiro
Russell, Steven
Ohtsuka, Satoshi
author_facet Niwa, Hitoshi
Nakamura, Akira
Urata, Makoto
Shirae-Kurabayashi, Maki
Kuraku, Shigehiro
Russell, Steven
Ohtsuka, Satoshi
author_sort Niwa, Hitoshi
collection PubMed
description BACKGROUND: In mouse ES cells, the function of Sox2 is essential for the maintenance of pluripotency. Since the Sox-family of transcription factors are well conserved in the animal kingdom, addressing the evolutionary origin of Sox2 function in pluripotent stem cells is intriguing from the perspective of understanding the origin of pluripotency. RESULTS: Here we approach this question using a functional complementation assay in inducible Sox2-null ES cells. Assaying mouse Sox proteins from different Groups, we found that only Group B1 and Group G proteins were able to support pluripotency. Interestingly, invertebrate homologs of mammalian Group B1 Sox proteins were able to replace the pluripotency-associated function of mouse Sox2. Moreover, the mouse ES cells rescued by the Drosophila SoxNeuro protein are able to contribute to chimeric embryos. CONCLUSIONS: These data indicate that the function of mouse Sox2 supporting pluripotency is based on an evolutionally conserved activity of the Group B1 Sox family. Since pluripotent stem cell population in developmental process could be regarded as the evolutional novelty in vertebrates, it could be regarded as a co-optional use of their evolutionally conserved function. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12862-016-0755-4) contains supplementary material, which is available to authorized users.
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spelling pubmed-50078702016-09-02 The evolutionally-conserved function of group B1 Sox family members confers the unique role of Sox2 in mouse ES cells Niwa, Hitoshi Nakamura, Akira Urata, Makoto Shirae-Kurabayashi, Maki Kuraku, Shigehiro Russell, Steven Ohtsuka, Satoshi BMC Evol Biol Research Article BACKGROUND: In mouse ES cells, the function of Sox2 is essential for the maintenance of pluripotency. Since the Sox-family of transcription factors are well conserved in the animal kingdom, addressing the evolutionary origin of Sox2 function in pluripotent stem cells is intriguing from the perspective of understanding the origin of pluripotency. RESULTS: Here we approach this question using a functional complementation assay in inducible Sox2-null ES cells. Assaying mouse Sox proteins from different Groups, we found that only Group B1 and Group G proteins were able to support pluripotency. Interestingly, invertebrate homologs of mammalian Group B1 Sox proteins were able to replace the pluripotency-associated function of mouse Sox2. Moreover, the mouse ES cells rescued by the Drosophila SoxNeuro protein are able to contribute to chimeric embryos. CONCLUSIONS: These data indicate that the function of mouse Sox2 supporting pluripotency is based on an evolutionally conserved activity of the Group B1 Sox family. Since pluripotent stem cell population in developmental process could be regarded as the evolutional novelty in vertebrates, it could be regarded as a co-optional use of their evolutionally conserved function. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12862-016-0755-4) contains supplementary material, which is available to authorized users. BioMed Central 2016-08-31 /pmc/articles/PMC5007870/ /pubmed/27582319 http://dx.doi.org/10.1186/s12862-016-0755-4 Text en © The Author(s). 2016 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research Article
Niwa, Hitoshi
Nakamura, Akira
Urata, Makoto
Shirae-Kurabayashi, Maki
Kuraku, Shigehiro
Russell, Steven
Ohtsuka, Satoshi
The evolutionally-conserved function of group B1 Sox family members confers the unique role of Sox2 in mouse ES cells
title The evolutionally-conserved function of group B1 Sox family members confers the unique role of Sox2 in mouse ES cells
title_full The evolutionally-conserved function of group B1 Sox family members confers the unique role of Sox2 in mouse ES cells
title_fullStr The evolutionally-conserved function of group B1 Sox family members confers the unique role of Sox2 in mouse ES cells
title_full_unstemmed The evolutionally-conserved function of group B1 Sox family members confers the unique role of Sox2 in mouse ES cells
title_short The evolutionally-conserved function of group B1 Sox family members confers the unique role of Sox2 in mouse ES cells
title_sort evolutionally-conserved function of group b1 sox family members confers the unique role of sox2 in mouse es cells
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5007870/
https://www.ncbi.nlm.nih.gov/pubmed/27582319
http://dx.doi.org/10.1186/s12862-016-0755-4
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