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Updated: May 18, 2026

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
Published on: June 6, 2017
The cell-cycle regulator c-Myc is essential for the formation and maintenance of germinal centers
Dinis Pedro Calado1, Yoshiteru Sasaki, Susana A Godinho
1Program of Cellular and Molecular Medicine, Children's Hospital, and Immune Disease Institute, Harvard Medical School, Boston, Massachusetts, USA. dinis.calado@mdc-berlin.de
Insights
This study reveals that c-Myc is essential for germinal center (GC) formation and maintenance. Identifying c-Myc positive B cells highlights their critical role and potential risk in B cell lymphoma development.
Area of Science:
- Immunology
- Cell Biology
- Oncology
Background:
- Germinal centers (GCs) are crucial for adaptive immunity, supporting B cell proliferation and antibody responses.
- The precise role of c-Myc, a key regulator of cell proliferation, within GCs has been unclear.
Purpose of the Study:
- To investigate the function of c-Myc in B cells within germinal centers.
- To determine the necessity of c-Myc for GC formation and maintenance.
Main Methods:
- Identification of c-Myc expressing B cell subpopulations in immature and mature GCs.
- Genetic ablation of the Myc gene to assess its impact on GC dynamics.
Main Results:
- Distinct c-Myc positive (c-Myc(+)) B cell subpopulations were identified in both immature and mature GCs.
- Genetic deletion of Myc demonstrated its indispensable role in GC formation and maintenance.
Conclusions:
- Specific c-Myc(+) B cell subsets are functionally critical for GC development and stability.
- These findings have significant implications for understanding B cell lymphomagenesis, particularly MYC-driven lymphomas originating from GC B cells.
- c-Myc(+) GC B cell subpopulations may represent a high-risk group for malignant transformation due to MYC translocation susceptibility.
Abstract:
Germinal centers (GCs) are sites of intense B cell proliferation and are central for T cell-dependent antibody responses. However, the role of c-Myc, a key cell-cycle regulator, in this process has been questioned. Here we identified c-Myc(+) B cell subpopulations in immature and mature GCs and found, by genetic ablation of Myc, that they had indispensable roles in the formation and maintenance of GCs. The identification of these functionally critical cellular subsets has implications for human B cell lymphomagenesis, which originates mostly from GC B cells and frequently involves MYC chromosomal translocations. As these translocations are generally dependent on transcription of the recombining partner loci, the c-Myc(+) GC subpopulations may be at a particularly high risk for malignant transformation.
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