AID Mediates Hypermutation by Deaminating Single Stranded DNA

doi:10.1084/jem.20030481

Published 19 May 2003. doi:10.1084/jem.20030481

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© Rockefeller University Press, 0022-1007/2003/5/1291 $5.00
The Journal of Experimental Medicine, Volume 197, Number 10, 1291-1296

AID Mediates Hypermutation by Deaminating Single Stranded DNA

Sarah K. Dickerson¹^,2, Eleonora Market¹^,2, Eva Besmer¹ and F. Nina Papavasiliou¹

¹ Laboratory of Lymphocyte Biology, New York, NY 10021
² The Rockefeller University Graduate School, New York, NY 10021

Address correspondence to F. Nina Papavasiliou, Laboratory of Lymphocyte Biology, 1230 York Ave., New York, NY 10021. Phone: 212-327-7857; Fax: 212-327-7319; E-mail: papavasiliou{at}rockefeller.edu

Activation-induced deaminase (AID) is a protein indispensablefor the diversification of immunoglobulin (Ig) genes by somatichypermutation (SHM), class switch recombination (CSR), and geneconversion. To date, the precise role of AID in these processeshas not been determined. Here we demonstrate that purified,tetrameric AID can deaminate cytidine residues in DNA, but notin RNA. Furthermore, we show that AID will bind and deaminateonly single-stranded DNA, which implies a direct, functionallink between hypermutation and transcription. Finally, AID doesnot target mutational hotspots, thus mutational targeting tospecific residues must be attributed to different factors.

Key Words: B lymphocytes • immunoglobulin gene • activation-induced deaminase • somatic hypermutation

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