Pre-B cell receptor-mediated activation of BCL6 induces pre-B cell quiescence 
through transcriptional repression of MYC

Nahar, Rahul; Ramezani-Rad, Parham; Mossner, Maximilian; Duy, Cihangir; Cherchietti, Leandro; Geng, Huimin; Dovat, Sinisa; Jumaa, Hassan; Ye, B. Hilda; Melnick, Ari; Müschen, Markus

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Pre-B cell receptor-mediated activation of BCL6 induces pre-B cell quiescence through transcriptional repression of MYC

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Jumaa, Hassan
Research Group and Chair of Molecular Immunology of the University of Freiburg, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Citation

Nahar, R., Ramezani-Rad, P., Mossner, M., Duy, C., Cherchietti, L., Geng, H., et al. (2011). Pre-B cell receptor-mediated activation of BCL6 induces pre-B cell quiescence through transcriptional repression of MYC. Blood, 118, 4174-4178.

Cite as: https://hdl.handle.net/11858/00-001M-0000-002B-8DBF-5

Abstract

Initial cell surface expression of the pre-B cell receptor induces proliferation. After 2 to 5 divisions, however, large pre-BII (Fraction C') cells exit cell cycle to become resting, small pre-BII cells (Fraction D). The mechanism by which pre-BII cells exit cell cycle, however, is currently unclear. The checkpoint at the Fraction C'-D transition is critical for immunoglobulin light chain gene recombination and to prevent malignant transformation into acute lymphoblastic leukemia. Here we demonstrate that inducible activation of pre-B cell receptor signaling induces cell-cycle exit through up-regulation of the transcriptional repressor BCL6. Inducible activation of BCL6 downstream of the pre-B cell receptor results in transcriptional repression of MYC and CCND2. Hence, pre-B cell receptor-mediated activation of BCL6 limits pre-B cell proliferation and induces cellular quiescence at the small pre-BII (Fraction D) stage.