Authors: Zhangguo Chen Jing H Wang
Publish Date: 2014/04/21
Volume: 8, Issue: 2, Pages: 201-216
Abstract
Activationinduced deaminase AID initiates the secondary antibody diversification process in B lymphocytes In mammalian B cells this process includes somatic hypermutation SHM and class switch recombination CSR both of which require AID AID induces UG mismatch lesions in DNA that are subsequently converted into point mutations or DNA double stranded breaks during SHM/CSR In a physiological context AID targets immunoglobulin Ig loci to mediate SHM/CSR However recent studies reveal genomewide access of AID to numerous nonIg loci Thus AID poses a threat to the genome of B cells if AIDinitiated DNA lesions cannot be properly repaired In this review we focus on the molecular mechanisms that regulate the specificity of AID targeting and the repair pathways responsible for processing AIDinitiated DNA lesions
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