AID Is Required for the Chromosomal Breaks in c-myc that Lead to c-myc/IgH Translocations | Zendy

Davide F. Robbiani | Zendy; Anne Bothmer | Zendy; Elsa Callén | Zendy; Bernardo ReinaSanMartin | Zendy; Yair Dorsett | Zendy; Simone Difilippantonio | Zendy; Daniel J. Bolland | Zendy; Hua Tang Chen | Zendy; Anne E. Corcoran | Zendy; André Nussenzweig | Zendy; Michel C. Nussenzweig | Zendy

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AID Is Required for the Chromosomal Breaks in c-myc that Lead to c-myc/IgH Translocations

Author(s) -

Davide F. Robbiani,

Anne Bothmer,

Elsa Callén,

Bernardo ReinaSanMartin,

Yair Dorsett,

Simone Difilippantonio,

Daniel J. Bolland,

Hua Tang Chen,

Anne E. Corcoran,

André Nussenzweig,

Michel C. Nussenzweig

Publication year - 2008

Publication title -

cell

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 26.304

H-Index - 776

eISSN - 1097-4172

pISSN - 0092-8674

DOI - 10.1016/j.cell.2008.09.062

Subject(s) - biology , somatic hypermutation , chromosomal translocation , cytidine deaminase , microbiology and biotechnology , immunoglobulin heavy chain , dna , activation induced (cytidine) deaminase , immunoglobulin class switching , gene , genetics , antibody , b cell

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.

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