Msh2 ATPase activity is essential for somatic hypermutation at a-T basepairs and for efficient class switch recombination.

ABSTRACT: Somatic hypermutation (SHM) and class switch recombination (CSR) are initiated by activation-induced cytidine deaminase-mediated cytidine deamination of immunoglobulin genes. MutS homologue (Msh) 2-/- mice have reduced A-T mutations and CSR. This suggests that Msh2 may play a role in repairing activation-induced cytidine deaminase-generated G-U mismatches. However, because Msh2 not only initiates mismatch repair but also has other functions, such as signaling for apoptosis, it is not known which activity of Msh2 is responsible for the effects observed, and consequently, many models have been proposed. To further dissect the role of Msh2 in SHM and CSR, mice with a "knockin" mutation in the Msh2 gene that inactivates the adenosine triphosphatase domain were examined. This mutation (i.e., Ms

SUBMITTER: Martin A 

PROVIDER: S-EPMC2194233 | biostudies-literature | 2003 Oct

REPOSITORIES: biostudies-literature