Transcription factor EBF1 is essential for the maintenance of B cell identity 
and prevention of alternative fates in committed cells

Nechanitzky, Robert; Akbas, Duygu; Scherer, Stefanie; Györy, Ildiko; Hoyler, Thomas; Ramamoorthy, Senthilkumar; Diefenbach, Andreas; Grosschedl, Rudolf

doi:10.1038/ni.2641

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Transcription factor EBF1 is essential for the maintenance of B cell identity and prevention of alternative fates in committed cells

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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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Akbas, Duygu
Department of Cellular and Molecular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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

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Györy, Ildiko
Department of Cellular and Molecular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Ramamoorthy, Senthilkumar
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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https://www.nature.com/articles/ni.2641
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Citation

Nechanitzky, R., Akbas, D., Scherer, S., Györy, I., Hoyler, T., Ramamoorthy, S., et al. (2013). Transcription factor EBF1 is essential for the maintenance of B cell identity and prevention of alternative fates in committed cells. Nature Immunology, 14, 867-875. doi:10.1038/ni.2641.

Cite as: https://hdl.handle.net/11858/00-001M-0000-002B-88E6-D

Abstract

The transcription factors EBF1 and Pax5 have been linked to activation of the B cell lineage program and irreversible loss of alternative lineage potential (commitment), respectively. Here we conditionally deleted Ebf1 in committed pro-B cells after transfer into alymphoid mice. We found that those cells converted into innate lymphoid cells (ILCs) and T cells with variable-diversity-joining (VDJ) rearrangements of loci encoding both B cell and T cell antigen receptors. As intermediates in lineage conversion, Ebf1-deficient CD19⁺ cells expressing Pax5 and transcriptional regulators of the ILC and T cell fates were detectable. In particular, genes encoding the transcription factors Id2 and TCF-1 were bound and repressed by EBF1. Thus, both EBF1 and Pax5 are required for B lineage commitment by repressing distinct and common determinants of alternative cell fates.