Competitive repair pathways in immunoglobulin gene hypermutation.
This review focuses on the contribution of translesion DNA polymerases to immunoglobulin gene hypermutation, in particular on the roles of DNA polymerase eta (Poleta) in the generation of mutations at A/T bases from the initial cytosine-targeted activation-induced cytidine deaminase (AID)-mediated deamination event, and of Polkappa, an enzyme of the same polymerase family, used as a substitute when Poleta is absent. The proposition that the UNG uracil glycosylase and the MSH2-MSH6 mismatch recognition complex are two competitive rather than alternative pathways in the processing of uracils generated by AID is further discussed.
Reynaud
Claude-Agnès
CA
INSERM U783 Développement du système immunitaire, Université Paris Descartes, Faculté de Médecine, Site Necker-Enfants Malades, 156 rue de Vaugirard, 75730 Paris Cedex 15, France.
Delbos
Frédéric
F
Faili
Ahmad
A
Guéranger
Quentin
Q
Aoufouchi
Said
S
Weill
Jean-Claude
JC
D003564:Cytidine Deaminase / Q000378:metabolism*; D004260:DNA Repair / Q000235:genetics / Q000276:immunology*; D004259:DNA-Directed DNA Polymerase / Q000378:metabolism*; D003641:Deamination; D051719:MutS DNA Mismatch-Binding Protein / Q000235:genetics / Q000378:metabolism; D027041:Somatic Hypermutation, Immunoglobulin / Q000235:genetics*; D051981:Uracil-DNA Glycosidase / Q000378:metabolism; D000099270:Y-Family DNA Polymerases
D003564:Cytidine Deaminase; D004259:DNA-Directed DNA Polymerase; D051719:MutS DNA Mismatch-Binding Protein; D051981:Uracil-DNA Glycosidase; C112338:Rad30 protein; D000099270:Y-Family DNA Polymerases