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Induction and Assessment of Class Switch Recombination in Purified Murine B Cells
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Published on: August 13, 2010

Differential programming of B cells in AID deficient mice

Marc A Hogenbirk1, Marinus R Heideman, Arno Velds

  • 1Division of Biological Stress Response, The Netherlands Cancer Institute, Amsterdam, The Netherlands.

Plos One
|August 8, 2013
PubMed

The Aicda locus encodes the activation induced cytidine deaminase (AID) and is highly expressed in germinal center (GC) B cells to initiate somatic hypermutation (SHM) and class switch recombination (CSR) of immunoglobulin (Ig) genes. Besides these Ig specific activities in B cells, AID has been implicated in active DNA demethylation in non-B cell systems. We here determined a potential role of AID as an epigenetic eraser and transcriptional regulator in B cells. RNA-Seq on different B cell subsets revealed that Aicda(-/-) B cells are developmentally affected. However as shown by RNA-Seq, MethylCap-Seq, and SNP analysis these transcriptome alterations may not relate to AID, but alternatively to a CBA mouse strain derived region around the targeted Aicda locus. These unexpected confounding parameters provide alternative, AID-independent interpretations on genotype-phenotype correlations previously reported in numerous studies on AID using the Aicda(-/-) mouse strain.

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