The Journal of Experimental Medicine
Torrey Pines Biolabs
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
Published 18 January 2005. doi:10.1084/jem.20040772
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 201, Number 2, 189-194
This Article
Right arrow Full Text
Right arrow Full Text (PDF, 320K)
Right arrow PPT slides of all figures
Right arrow Supplemental Material Index
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 Pan-Hammarström, Q.
Right arrow Articles by Ehrenstein, M. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Pan-Hammarström, Q.
Right arrow Articles by Ehrenstein, M. R.
Right arrowPubmed/NCBI databases
*Substance via MeSH
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

 Impact of DNA ligase IV on nonhomologous end joining pathways during class switch recombination in human cells

Qiang Pan-Hammarström1, Anne-Marie Jones2, Aleksi Lähdesmäki1, Wei Zhou1, Richard A. Gatti3, Lennart Hammarström1, Andrew R. Gennery4, and Michael R. Ehrenstein2

1 Clinical Immunology, Department of Laboratory Medicine, Karolinska University Hospital Huddinge, SE-14186 Stockholm, Sweden
2 Department of Medicine, University College London, London W1T 4NJ, England, UK
3 Department of Pathology, University of California Los Angeles School of Medicine, CA 90095
4 Department of Pediatric Immunology, Newcastle General Hospital, Newcastle NE4 6BE, England, UK

CORRESPONDENCE Michael Ehrenstein: m.ehrenstein{at}ucl.ac.uk or Qiang Pan-Hammarström: Qiang.Pan-Hammarstrom{at}labmed.ki.se

Class switch recombination (CSR) is a region-specific, transcriptionally regulated, nonhomologous recombinational process that is initiated by activation-induced cytidine deaminase (AID). The initial lesions in the switch (S) regions are subsequently processed and resolved, leading to recombination of the two targeted S regions. The mechanisms by which repair and ligation of the broken DNA ends occurs is still elusive. Recently, a small number of patients lacking DNA ligase IV, a critical component of the nonhomologous end joining (NHEJ) machinery, have been identified. We show that these patients display a considerably increased donor/acceptor homology at Sµ–S{alpha} junctions compared with healthy controls. In contrast, Sµ–S{gamma} junctions show an increased frequency of insertions but no increase in junctional homology. These altered patterns of junctional resolution may be related to differences in the homology between the Sµ and the downstream isotype S regions, and could reflect different modes of switch junction resolution when NHEJ is impaired. These findings link DNA ligase IV, and thus NHEJ, to CSR.


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