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Satb1 and Satb2 Are Dispensable for X Chromosome Inactivation in Mice

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Nechanitzky,  Robert
Department of Cellular and Molecular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Dávila,  Amparo
Department of Cellular and Molecular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Savarese,  Fabio
Department of Cellular and Molecular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Fietze,  Stefanie
Department of Cellular and Molecular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Grosschedl,  Rudolf
Department of Cellular and Molecular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Citation

Nechanitzky, R., Dávila, A., Savarese, F., Fietze, S., & Grosschedl, R. (2012). Satb1 and Satb2 Are Dispensable for X Chromosome Inactivation in Mice. Developmental Cell, 23, 866-871. doi:10.1016/j.devcel.2012.09.018.


Cite as: https://hdl.handle.net/11858/00-001M-0000-002B-8CC0-3
Abstract
Satb1 and Satb2 have been recently described as regulators of embryonic stem (ES) cell pluripotency and as silencing factors in X chromosome inactivation. The influence of the pluripotency machinery on X chromosome inactivation and the lack of an X chromosome inactivation defect in Satb1-/- and Satb2-/- mice raise the question of whether or not Satb proteins are directly and/or redundantly involved in this process. Here, we analyzed X chromosome inactivation in fibroblastic cells that were derived from female Satb1-/-Satb2-/- embryos. By fluorescence in situ hybridization to visualize Xist RNA and by immunohistochemistry to detect H3K27me3 histone modifications, we found that female Satb1-/-Satb2-/- fibroblastic cells contain proper Barr bodies. Moreover, we did not detect an upregulation of X-linked genes, suggesting that Satb proteins are dispensable for X chromosome inactivation in mice.