Induction of somatic hypermutation in immunoglobulin genes is dependent on DNA polymerase iota

Ahmad Faili, Said Aoufouchi, Eric Flatter, Quentin Guéranger, Claude-Agnès Reynaud and Jean-Claude Weill ()
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Ahmad Faili: INSERM U373, Faculté de Médecine Necker-Enfants Malades
Said Aoufouchi: INSERM U373, Faculté de Médecine Necker-Enfants Malades
Eric Flatter: INSERM U373, Faculté de Médecine Necker-Enfants Malades
Quentin Guéranger: INSERM U373, Faculté de Médecine Necker-Enfants Malades
Claude-Agnès Reynaud: INSERM U373, Faculté de Médecine Necker-Enfants Malades
Jean-Claude Weill: INSERM U373, Faculté de Médecine Necker-Enfants Malades

Nature, 2002, vol. 419, issue 6910, 944-947

Abstract: Abstract Somatic hypermutation of immunoglobulin genes is a unique, targeted, adaptive process. While B cells are engaged in germinal centres in T-dependent responses, single base substitutions are introduced in the expressed V h/V l genes to allow the selection of mutants with a higher affinity for the immunizing antigen. Almost every possible DNA transaction has been proposed to explain this process, but each of these models includes an error-prone DNA synthesis step that introduces the mutations1,2. The Y family of DNA polymerases3—pol η, pol ι, pol κ and rev1—are specialized for copying DNA lesions and have high rates of error when copying a normal DNA template4,5. By performing gene inactivation in a Burkitt's lymphoma cell line inducible for hypermutation, we show here that somatic hypermutation is dependent on DNA polymerase iota.

Date: 2002
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DOI: 10.1038/nature01117

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