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Specific erythroid-lineage defect in mice conditionally deficient for Mediator subunit Med1

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Stumpf,  Melanie
Department of Cellular and Molecular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Yue,  Xiaojing
Department of Cellular and Molecular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Schmitz,  Sandra
Department of Cellular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Borggrefe,  Tilman
Department of Cellular and Molecular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Citation

Stumpf, M., Yue, X., Schmitz, S., Luche, H., Reddy, J. K., & Borggrefe, T. (2010). Specific erythroid-lineage defect in mice conditionally deficient for Mediator subunit Med1. Proceedings of the National Academy of Sciences U.S.A., 50, 21541-21546.


Cite as: http://hdl.handle.net/11858/00-001M-0000-002B-8EDE-8
Abstract
The Mediator complex forms the bridge between transcriptional activators and the RNA polymerase II. Med1 (also known as PBP or TRAP220) is a key component of Mediator that interacts with nuclear hormone receptors and GATA transcription factors. Here, we show dynamic recruitment of GATA-1, TFIIB, Mediator, and RNA polymerase II to the β-globin locus in induced mouse erythoid leukemia cells and in an erythropoietin-inducible hematopoietic progenitor cell line. Using Med1 conditional knockout mice, we demonstrate a specific block in erythroid development but not in myeloid or lymphoid development, highlighted by the complete absence of β-globin gene expression. Thus, Mediator subunit Med1 plays a pivotal role in erythroid development and in β-globin gene activation.