The Journal of Experimental Medicine
Accuri Cytometers
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Published 18 January 2005. doi:10.1084/jem.20040772
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 201, Number 2, 189-194
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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.


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