B cell development leads off with a base hit: dU:dG mismatches in class switching and hypermutation.
The mechanisms underlying somatic hypermutation (SHM) and class switch recombination (CSR) have been the subject of much debate. Recent studies from the Neuberger and Honjo labs have lent insight into these distinct processes, and we discuss a new, comprehensive model for how AID, uracil DNA glycosylase (UNG) and the mismatch repair system function in both SHM and CSR.
Lee
Gregory S
GS
Skirball Institute of Biomolecular Medicine, Department of Pathology, New York University School of Medicine, New York, New York 10016, USA.
Brandt
Vicky L
VL
Roth
David B
DB
D000818:Animals; D001402:B-Lymphocytes / Q000201:enzymology / Q000276:immunology / Q000378:metabolism*; D020137:Base Pair Mismatch / Q000276:immunology; D003564:Cytidine Deaminase / Q000378:metabolism; D045647:DNA Glycosylases / Q000378:metabolism; D004260:DNA Repair; D006801:Humans; D017578:Immunoglobulin Class Switching / Q000235:genetics*; D018448:Models, Immunological; D017393:RNA Editing; D027041:Somatic Hypermutation, Immunoglobulin / Q000235:genetics*; D051981:Uracil-DNA Glycosidase
D045647:DNA Glycosylases; D051981:Uracil-DNA Glycosidase; D003564:Cytidine Deaminase