UNG shapes the specifity of AID-induced somatic hypermutation in B cells

ABSTRACT: Secondary diversification of antibodies through somatic hypermutation (SHM) and class switch recombination (CSR) is a critical component of the immune response. Activation-induced deaminase (AID) initiates both processes by deaminating cytosine residues in immunoglobulin genes. The resulting U:G mismatch can be processed by alternative pathways to give rise to a mutation (SHM) or a DNA double-strand break (CSR). Central to this processing is the activity of uracil-N-glycosylase (UNG), an enzyme normally involved in error-free base excision repair. We used next generation sequencing to analyze the contribution of UNG to the resolution of AID-induced lesions. Loss- and gain-of-function experiments showed that UNG activity can promote both error-prone and high fidelity repair of U:G lesions.

ORGANISM(S): Mus musculus

SUBMITTER: Pablo Perez-Duran 

PROVIDER: E-GEOD-39114 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress