Eukaryotic Cell
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Other Versions of this Article:
EC.00212-07v1
6/10/1773    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Burton, P.
Right arrow Articles by McCulloch, R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Burton, P.
Right arrow Articles by McCulloch, R.
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.

Ku Heterodimer-Independent End Joining in Trypanosoma brucei Cell Extracts Relies upon Sequence Microhomology{triangledown}

Peter Burton, David J. McBride, Jonathan M. Wilkes, J. David Barry, and Richard McCulloch*

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.


* Corresponding author. Mailing address: The Wellcome Centre for Molecular Parasitology, University of Glasgow, Glasgow Biomedical Research Centre, 120 University Place, Glasgow, G12 8TA, Scotland. Phone: 44-141-330-5946. Fax: 44-141-330-5422. E-mail: rmc9z{at}udcf.gla.ac.uk

{triangledown} Published ahead of print on 10 August 2007.


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.




This article has been cited by other articles:




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Appl. Environ. Microbiol. Infect. Immun. J. Bacteriol.
Mol. Cell Biol. Microbiol. Mol. Biol. Rev. ALL ASM JOURNALS
Copyright © 2007 by the American Society for Microbiology.