Related Experiment Video
Updated: May 3, 2026

Recombinant Retroviral Production and Infection of B Cells
Published on: February 19, 2011
AID is required for the chromosomal breaks in c-myc that lead to c-myc/IgH translocations
Davide F Robbiani1, Anne Bothmer, Elsa Callen
1Laboratory of Molecular Immunology, The Rockefeller University, New York, NY 10065, USA.
Abstract:
Chromosomal translocation requires formation of paired double-strand DNA breaks (DSBs) on heterologous chromosomes. One of the most well characterized oncogenic translocations juxtaposes c-myc and the immunoglobulin heavy-chain locus (IgH) and is found in Burkitt's lymphomas in humans and plasmacytomas in mice. DNA breaks in IgH leading to c-myc/IgH translocations are created by activation-induced cytidine deaminase (AID) during antibody class switch recombination or somatic hypermutation. However, the source of DNA breaks at c-myc is not known. Here, we provide evidence for the c-myc promoter region being required in targeting AID-mediated DNA damage to produce DSBs in c-myc that lead to c-myc/IgH translocations in primary B lymphocytes. Thus, in addition to producing somatic mutations and DNA breaks in antibody genes, AID is also responsible for the DNA lesions in oncogenes that are required for their translocation.
Related Concept Videos
DNA Damage can Stall the Cell Cycle
M-Cdk Drives Transition Into Mitosis
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
Abnormal Proliferation
Separation of Sister Chromatids
At the onset of anaphase, separase, a proteolytic enzyme, is...
Anaphase Promoting Complex
Induced Pluripotent Stem Cells
Somatic...

