| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 3345965 | Current Opinion in Immunology | 2011 | 8 Pages |
Abstract
Post-rearrangement diversification of the antibody repertoire relies on a DNA editing factor, the cytidine deaminase AID. How B lymphocytes avoid generalized mutagenesis while expressing high levels of AID remained a long-standing question. Genome-wide studies of AID targeting combined to the discovery of several co-factors controlling its recruitment and its local activity shed new light on this enigma.
► Large scale sequencing shows that AID binds and deaminates thousands of loci. ► AID is recruited to its targets by RNA Pol II stalling, via its interaction with Spt5. ► Interaction with the RNA exosome licenses AID access to the transcribed strand. ► Off-targeting produces DNA breaks at various loci, even in non-transcribed regions.
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Authors
Sébastien Storck, Said Aoufouchi, Jean-Claude Weill, Claude-Agnès Reynaud,