MCB
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Supplemental material
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Besmer, E.
Right arrow Articles by Papavasiliou, F. N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Besmer, E.
Right arrow Articles by Papavasiliou, F. N.
Molecular and Cellular Biology, June 2006, p. 4378-4385, Vol. 26, No. 11
0270-7306/06/$08.00+0     doi:10.1128/MCB.02375-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

The Transcription Elongation Complex Directs Activation-Induced Cytidine Deaminase-Mediated DNA Deamination{dagger}

Eva Besmer, Eleonora Market, and F. Nina Papavasiliou*

Laboratory of Lymphocyte Biology, The Rockefeller University, 1230 York Avenue, New York, New York 10021

Received 13 December 2005/ Returned for modification 27 January 2006/ Accepted 17 March 2006

Activation-induced cytidine deaminase (AID) is a single-stranded DNA deaminase required for somatic hypermutation of immunoglobulin (Ig) genes, a key process in the development of adaptive immunity. Transcription provides a single-stranded DNA substrate for AID, both in vivo and in vitro. We present here an assay which can faithfully replicate all of the molecular features of the initiation of hypermutation of Ig genes in vivo. In this assay, which detects AID-mediated deamination in the context of transcription by Escherichia coli RNA polymerase, deamination targets either strand and declines in efficiency as the distance from the promoter increases. We show that AID binds DNA exposed by the transcribing polymerase, implicating the polymerase itself as the vehicle which distributes AID on DNA as it moves away from the promoter.


* Corresponding author. Mailing address: Laboratory of Lymphocyte Biology, The Rockefeller University, 1230 York Avenue, New York, NY 10021. Phone: (212) 327-7857. Fax: (212) 327-7319. E-mail: papavasiliou{at}rockefeller.edu.

{dagger} Supplemental material for this article may be found at http://mcb.asm.org/.


Molecular and Cellular Biology, June 2006, p. 4378-4385, Vol. 26, No. 11
0270-7306/06/$08.00+0     doi:10.1128/MCB.02375-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:




Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. J. Virol. Eukaryot. Cell
Microbiol. Mol. Biol. Rev. Clin. Vaccine Immunol. All ASM Journals

Copyright © 2006 by the American Society for Microbiology. All rights reserved.