Abstract
Ig class switch recombination (CSR) and somatic hypermutation require activation-induced cytidine deaminase (AID). The search for AID-interaction factors has been a major research effort in the field, as the mechanism of preferential targeting of AID to Ig loci remains elusive. CTNNBL1 is one of the few identified AID-interacting factors and has been shown to affect AID-mediated mutation and gene conversion in chicken DT40 cells. CTNNBL1 was also implicated in mammalian CSR by the fact that an AID mutant that fails to interact with CTNNBL1 also fails to support CSR in AID-deficient mouse B cells. To directly assess the role of CTNNBL1 in CSR, we disrupted the CTNNBL1 gene on both alleles in mouse CH12F3 cells by gene targeting. We found normal levels of CSR in CTNNBL1-deficient cells, indicating that CTNNBL1 is dispensable for CSR.
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