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Eukaryotic Cell, October 2007, p. 1773-1781, Vol. 6, No. 10
1535-9778/07/$08.00+0 doi:10.1128/EC.00212-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

The Wellcome Centre for Molecular Parasitology, University of Glasgow, Glasgow Biomedical Research Centre, 120 University Place, Glasgow, G12 8TA, Scotland
Received 19 June 2007/ Accepted 1 August 2007
DNA double-strand breaks (DSBs) are repaired primarily by two distinct pathways: homologous recombination and nonhomologous end joining (NHEJ). NHEJ has been found in all eukaryotes examined to date and has been described recently for some bacterial species, illustrating its ancestry. Trypanosoma brucei is a divergent eukaryotic protist that evades host immunity by antigenic variation, a process in which homologous recombination plays a crucial function. While homologous recombination has been examined in some detail in T. brucei, little work has been done to examine what other DSB repair pathways the parasite utilizes. Here we show that T. brucei cell extracts support the end joining of linear DNA molecules. These reactions are independent of the Ku heterodimer, indicating that they are distinct from NHEJ, and are guided by sequence microhomology. We also demonstrate bioinformatically that T. brucei, in common with other kinetoplastids, does not encode recognizable homologues of DNA ligase IV or XRCC4, suggesting that NHEJ is either absent or mechanistically diverged in these pathogens.
Published ahead of print on 10 August 2007.
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