Transcriptional stalling in B-lymphocytes

Abstract

B cells utilize three DNA alteration strategies—V(D)J recombination, somatic hypermutation (SHM) and class switch recombination (CSR)—to somatically mutate their genome, thereby expressing a plethora of antibodies tailor-made against the innumerable antigens they encounter while in circulation. Of these three events, the single-strand DNA cytidine deaminase, Activation Induced cytidine Deaminase (AID), is responsible for SHM and CSR. Recent advances, discussed in this review article, point toward various components of RNA polymerase II “stalling” machinery as regulators of AID activity during antibody diversification and maintenance of B cell genome integrity.

Keywords: :

• Activation Induced Deaminase
• somatic mutation
• RNA polymerase II regulation

Disclosure of Potential Conflicts of Interest

No potential conflicts of interest were disclosed.

Acknowledgments

We thank Dr. Rushad Pavri (IMP, Vienna) for critical input on the manuscript. This work was supported by funding from the National Institutes of Health Director’s office (1DP2OD008651–01) and the National Institute of Allergy and Infectious Diseases (1R01AI099195–01A1).