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  Satb1 and Satb2 regulate embryonic stem cell differentiation and Nanog expression

Savarese, F., Dávila, A., Nechanitzky, R., De La Rosa-Velazquez, I., Pereira, C. F., Engelke, R., et al. (2009). Satb1 and Satb2 regulate embryonic stem cell differentiation and Nanog expression. Genes & Development, 23, 2625-2638.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-002B-8FA1-6 Version Permalink: http://hdl.handle.net/11858/00-001M-0000-002B-8FA2-4
Genre: Journal Article

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 Creators:
Savarese, Fabio1, Author              
Dávila, Amparo1, Author              
Nechanitzky, Robert1, Author              
De La Rosa-Velazquez, Inti2, Author
Pereira, Carlos F., Author
Engelke, Rudolf1, Author              
Takahashi, Keiko, Author
Jenuwein, Thomas3, Author              
Kohwi-Shigematsue, Terumi, Author
Fisher, Amanda, Author
Grosschedl, Rudolf1, Author              
Affiliations:
1Department of Cellular and Molecular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243641              
2Max Planck Society, ou_persistent13              
3Department of Epigenetics, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243644              

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Free keywords: Embryonic stem cells, pluripotency, differentiation, Satb1, Satb2, Nanog
 Abstract: Satb1 and the closely related Satb2 proteins regulate gene expression and higher-order chromatin structure of multigene clusters in vivo. In examining the role of Satb proteins in murine embryonic stem (ES) cells, we find that Satb1-/- cells display an impaired differentiation potential and augmented expression of the pluripotency determinants Nanog, Klf4, and Tbx3. Metastable states of self-renewal and differentiation competence have been attributed to heterogeneity of ES cells in the expression of Nanog. Satb1-/- cultures have a higher proportion of Nanog(high) cells, and an increased potential to reprogram human B lymphocytes in cell fusion experiments. Moreover, Satb1-deficient ES cells show an increased expression of Satb2, and we find that forced Satb2 expression in wild-type ES cells antagonizes differentiation-associated silencing of Nanog and enhances the induction of NANOG in cell fusions with human B lymphocytes. An antagonistic function of Satb1 and Satb2 is also supported by the almost normal differentiation potential of Satb1-/-Satb2-/- ES cells. Taken together with the finding that both Satb1 and Satb2 bind the Nanog locus in vivo, our data suggest that the balance of Satb1 and Satb2 contributes to the plasticity of Nanog expression and ES cell pluripotency.

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Language(s): eng - English
 Dates: 2009
 Publication Status: Published in print
 Pages: -
 Publishing info: -
 Table of Contents: -
 Rev. Type: Peer
 Identifiers: eDoc: 464563
 Degree: -

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Title: Genes & Development
Source Genre: Journal
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Publ. Info: -
Pages: - Volume / Issue: 23 Sequence Number: - Start / End Page: 2625 - 2638 Identifier: -