The Journal of Experimental Medicine
VeriKine-HS Human IFN-Beta
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
Published online 13 June 2005 doi:10.1084/jem.20042491
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 201, Number 12, 1885-1890
This Article
Right arrow Full Text
Right arrow Full Text (PDF, 511K)
Right arrow PPT slides of all figures
Right arrow Alert me when this article is cited
Right arrow Citation Map
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new content in the JEM
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Min, I. M.
Right arrow Articles by Selsing, E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Min, I. M.
Right arrow Articles by Selsing, E.
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Facebook   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?

BRIEF DEFINITIVE REPORT

 Shifts in targeting of class switch recombination sites in mice that lack µ switch region tandem repeats or Msh2

Irene M. Min1, Lisa R. Rothlein2, Carol E. Schrader3,4, Janet Stavnezer3,4, and Erik Selsing1,2

1 Genetics Program, Tufts University School of Medicine, Boston, MA 02111
2 Department of Pathology, Tufts University School of Medicine, Boston, MA 02111
3 Program in Immunology and Virology, University of Massachusetts Medical School, Worcester, MA 01655
4 Department of Molecular Genetics and Microbiology, University of Massachusetts Medical School, Worcester, MA 01655

CORRESPONDENCE Erik Selsing: erik.selsing{at}tufts.edu

The mechanisms that target class switch recombination (CSR) to antibody gene switch (S) regions are unknown. Analyses of switch site locations in wild-type mice and in mice that lack the Sµ tandem repeats show shifts indicating that a 4–5-kb DNA domain (bounded upstream by the Iµ promoter) is accessible for switching independent of Sµ sequences. This CSR-accessible domain is reminiscent of the promoter-defined domains that target somatic hypermutation. Within the 4–5-kb CSR domain, the targeting of S site locations also depends on the Msh2 mismatch repair protein because Msh2-deficient mice show an increased focus of sites to the Sµ tandem repeat region. We propose that Msh2 affects S site location because sequences with few activation-induced cytidine deaminase targets generate mostly switch DNA cleavages that require Msh2-directed processing to allow CSR joining.


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


This article has been cited by other articles:



  Home | Help | Feedback | Subscriptions | Archive | Search
TABLE OF CONTENTS