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Induction and Assessment of Class Switch Recombination in Purified Murine B Cells
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
Summary
Activation induced cytidine deaminase (AID) plays a role in immunoglobulin gene mutation and may affect DNA demethylation. However, studies using AID-deficient mice may be confounded by genetic background, impacting genotype-phenotype correlations.
Area of Science:
- Immunology
- Epigenetics
- Molecular Biology
Background:
- The activation induced cytidine deaminase (AID) is crucial for immunoglobulin gene diversification in B cells.
- AID initiates somatic hypermutation (SHM) and class switch recombination (CSR) in germinal center (GC) B cells.
- Beyond B cells, AID has been suggested to function in DNA demethylation.
Purpose of the Study:
- To investigate the role of AID as an epigenetic eraser and transcriptional regulator in B cells.
- To re-evaluate genotype-phenotype correlations in studies using AID-deficient mice.
Main Methods:
- RNA-Sequencing (RNA-Seq) on various B cell subsets.
- Methylation Capture Sequencing (MethylCap-Seq).
- Single Nucleotide Polymorphism (SNP) analysis.
Main Results:
- Aicda-deficient (Aicda(-/-)) B cells exhibited developmental alterations.
- Transcriptome changes in Aicda(-/-) B cells were potentially attributed to a CBA mouse strain-derived region near the targeted Aicda locus, not AID itself.
- SNP analysis confirmed the presence of confounding genetic elements.
Conclusions:
- Developmental effects observed in Aicda(-/-) B cells may be independent of AID function.
- Confounding genetic parameters in the Aicda(-/-) mouse strain necessitate re-interpretation of previous findings.
- Alternative explanations exist for genotype-phenotype correlations in AID research.
