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Therefore, AID is haploinsufficient for antibody diversification and chromosome translocations.
Altogether these data indicate that AID is haploinsufficient for antibody diversification.
AID is specifically induced in germinal center B cells to carry out somatic hypermutation and class-switch recombination, which are two processes that are responsible for antibody diversification.
AID is a key enzyme for antibody diversification and due to its mutagenic activity outside immunoglobulin loci it is implicated in lymphomagenesis.
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It is expressed in germinal center B cells and is essential for the events of class switch recombination and somatic hypermutation during the process of antibody diversification [ 26– 28].
The error-prone DNA repair of uracil residues is thought to be responsible for the generation of A/T mutations during antibody diversification in B cells by the activation-induced cytosine deaminase (AID) enzyme [19].
The requirement for CIB1 in AID-mediated processes was examined in two model systems for antibody gene diversification, the chicken B cell line DT40 and murine B lymphocytes.
The DNA cytosine deaminase activity of AID is essential for antibody gene diversification through the distinct processes of somatic hypermutation and class switch recombination [ 16].
We also uncover a potential mechanistic explanation for the targeting and off-target preferences of the antibody diversification mutator AID.
Neuberger, M. S. Antibody diversification by somatic mutation: from Burnet onwards.
Basu, U. et al. The AID antibody diversification enzyme is regulated by protein kinase A phosphorylation.
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