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Reassessing genomic targeting of AID

Nature Immunology volume 13, pages 797–798 (2012)Cite this article

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To the Editor:

The activation-induced cytidine deaminase AID (encoded by Aicda) is essential in triggering the somatic hypermutation, gene conversion and class-switch recombination of genes encoding immunoglobulins1. In an article published in Nature Immunology, Yamane et al. addressed a central issue in AID biology2. Applying chromatin immunoprecipitation followed by deep sequencing (ChIP-Seq) to primary, switch-induced B cells, they set out to establish the chromatin-binding 'preferences' of this DNA modifier. Using ChIP-Seq to identify genomic targets of AID is not trivial, given that AID is not a true chromatin-associated protein. Most AID is retained in the cytosol and only a small portion of the AID pool is actively shuttled between the cytoplasm and nucleus1. Of the nuclear fraction, only a small proportion is expected to interact with chromatin. Hence, extensive controls are needed for measurement of specific enrichment of the minor chromatin-bound AID fraction in Aicda+/+ B cells relative to its absence in Aicda−/− B cells. Here we argue that the ChIP-Seq data provided do not support the authors' conclusions2.

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Figure 1: Analysis of ChIP-Seq libraries of switch-induced Aicda+/+ and Aicda−/− B cells.

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Acknowledgements

Supported by the Dutch Cancer Foundation (M.A.H.; NKI-2008-4112 to H.J.).

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Authors and Affiliations

  1. Divison of Immunology, The Netherlands Cancer Institute, Amsterdam, The Netherlands

    Marc A Hogenbirk & Heinz Jacobs

  2. Genomic Core Facility, The Netherlands Cancer Institute, Amsterdam, The Netherlands

    Arno Velds & Ron M Kerkhoven

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  1. Marc A Hogenbirk
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  2. Arno Velds
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  3. Ron M Kerkhoven
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  4. Heinz Jacobs
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Correspondence to Marc A Hogenbirk or Heinz Jacobs.

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Hogenbirk, M., Velds, A., Kerkhoven, R. et al. Reassessing genomic targeting of AID. Nat Immunol 13, 797–798 (2012). https://doi.org/10.1038/ni.2367

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