Splice variants of activation induced deaminase (AID) do not affect the efficiency of class switch recombination in murine CH12F3 cells

• Published in: PloS one Vol. 10; no. 3; p. e0121719
• Main Authors: Sala, Cesare, Mattiuz, Giorgio, Pietrobono, Silvia, Chicca, Andrea, Conticello, Silvestro G
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 24-03-2015; Public Library of Science (PLoS)
• Subjects: Activation; Alternative splicing; Animals; B cells; Cell Line, Tumor; Class switching; Cloning; Cytidine Deaminase - genetics; Cytidine Deaminase - metabolism; Deoxyribonucleic acid; Diversification; DNA; DNA damage; Efficiency; Enzymes; Flow cytometry; Immunoglobulin Class Switching - genetics; Immunoglobulins; Laboratories; Leukemia; Lymphocytes B; Lymphoma; Mice; Mutation; Non-Hodgkin's lymphomas; Penicillin; Plasmids; Protein Isoforms - genetics; Protein Isoforms - metabolism; Proteins; Recombination; Recombination, Genetic; Regulation; Ribonucleic acid; RNA; Tumors; Italy; Switzerland
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0121719

Activation Induced Deaminase (AID) triggers the antigen-driven antibody diversification processes through its ability to edit DNA. AID dependent DNA damage is also the cause of genetic alterations often found in mature B cell tumors. A number of splice variants of AID have been identified, for which a role in the modulation of its activity has been hypothesized. We have thus tested two of these splice variants, which we find catalytically inactive, for their ability to modulate the activity of endogenous AID in CH12F3 cells, a murine lymphoma cell line in which Class Switch Recombination (CSR) can be induced. In contrast to full-length AID, neither these splice variants or a catalytically impaired AID mutant affect the efficiency of Class Switch Recombination. Thus, while a role for these splice variants at the RNA level remains possible, it is unlikely that they exert any regulatory effect on the function of AID.