Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents

This Article Full Text Full Text (PDF, 7920K) PDF+supp data (28732K) PPT slides of all figures Supplemental Material Index Alert me when this article is cited Citation Map Services Email this article Similar articles in this journal Similar articles in PubMed Alert me to new content in the JEM Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Shen, H. M. Articles by Storb, U. Search for Related Content PubMed PubMed Citation Articles by Shen, H. M. Articles by Storb, U. Social Bookmarking                            What's this?

¹ Department of Molecular Genetics and Cell Biology and ² Department of Medicine, University of Chicago, Chicago, IL 60637
³ Department of Physics and ⁴ Department of Biochemistry, Ohio State University, Columbus, OH 43210
⁵ Department of Biochemistry, Molecular Biology, and Cell Biology, Northwestern University, Evanston, IL 60208

CORRESPONDENCE Ursula Storb: stor{at}uchicago.edu

The activation-induced cytidine deaminase (AID) initiates somatic hypermutation, class-switch recombination, and gene conversion of immunoglobulin genes. In vitro, AID has been shown to target single-stranded DNA, relaxed double-stranded DNA, when transcribed, or supercoiled DNA. To simulate the in vivo situation more closely, we have introduced two copies of a nucleosome positioning sequence, MP2, into a supercoiled AID target plasmid to determine where around the positioned nucleosomes (in the vicinity of an ampicillin resistance gene) cytidine deaminations occur in the absence or presence of transcription. We found that without transcription nucleosomes prevented cytidine deamination by AID. However, with transcription AID readily accessed DNA in nucleosomes on both DNA strands. The experiments also showed that AID targeting any DNA molecule was the limiting step, and they support the conclusion that once targeted to DNA, AID acts processively in naked DNA and DNA organized within transcribed nucleosomes.

© 2009 Shen et al.
This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jem.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

CiteULike    Complore    Connotea    Del.icio.us    Digg    Facebook    Reddit    Technorati    Twitter    What's this?

This article has been cited by other articles:

• Chelico, L., Pham, P., Petruska, J., Goodman, M. F. (2009). Biochemical Basis of Immunological and Retroviral Responses to DNA-targeted Cytosine Deamination by Activation-induced Cytidine Deaminase and APOBEC3G. J. Biol. Chem. 284: 27761-27765 [Abstract] [Full Text]  
• Shen, H. M., Poirier, M. G., Allen, M. J., North, J., Lal, R., Widom, J., Storb, U. (2009). The activation-induced cytidine deaminase (AID) efficiently targets DNA in nucleosomes but only during transcription. JCB 185: i5-i5 [Full Text]  

Home | Help | Feedback | Subscriptions | Archive | Search

TABLE OF CONTENTS