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

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

Research output: Contribution to journalArticlepeer-review

43 Scopus citations

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 upregulation 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.

Original languageEnglish (US)
Pages (from-to)4174-4178
Number of pages5
JournalBlood
Volume118
Issue number15
DOIs
StatePublished - Oct 13 2011

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Immunology
  • Hematology
  • Cell Biology

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