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J. Biol. Chem., Vol. 277, Issue 29, 26185-26193, July 19, 2002
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,
From the Wellcome Centre for Molecular Parasitology, University of
Glasgow, Anderson College, 56 Dumbarton Road,
Glasgow G11 6NU, Scotland, United Kingdom
We demonstrate, by gene deletion analysis, that
Mre11 has a critical role in maintaining genomic integrity in
Trypanosoma brucei. mre11
/ null
mutant strains exhibited retarded growth but no delay or disruption of
cell cycle progression. They showed also a weak hyporecombination
phenotype and the accumulation of gross chromosomal rearrangements,
which did not involve sequence translocation, telomere loss, or
formation of new telomeres. The trypanosome mre11/ strains were hypersensitive to
phleomycin, a mutagen causing DNA double strand breaks (DSBs) but, in
contrast to mre11/ null mutants in other
organisms and T. brucei rad51/
null mutants, displayed no hypersensitivity to methyl methanesulfonate, which causes point mutations and DSBs. Mre11 therefore is important for
the repair of chromosomal damage and DSBs in trypanosomes, although in
this organism the intersection of repair pathways appears to differ
from that in other organisms. Mre11 inactivation appears not to affect
VSG gene switching during antigenic variation of a
laboratory strain, which is perhaps surprising given the importance of
homologous recombination during this process.
Present address: MRC Cancer Cell Unit, The Hutchison/MRC Centre,
Hills Road, Cambridge, CB2 2QH, UK.
§
Royal Society University Research Fellow.
¶
Wellcome Trust Principal Research Fellow. To whom
correspondence should be addressed: Wellcome Centre for Molecular
Parasitology, University of Glasgow, Anderson College, 56 Dumbarton
Rd., Glasgow, G11 6NU, Scotland, UK. Tel.: 44-141-330-4875; Fax:
44-141-330-5422; E-mail: j.d.barry@bio.gla.ac.uk.
This article has been cited by other articles:
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  L. Glover, R. McCulloch, and D. Horn Sequence homology and microhomology dominate chromosomal double-strand break repair in African trypanosomes Nucleic Acids Res., May 1, 2008; 36(8): 2608 - 2618. [Abstract] [Full Text] [PDF]
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 P. Burton, D. J. McBride, J. M. Wilkes, J. D. Barry, and R. McCulloch Ku Heterodimer-Independent End Joining in Trypanosoma brucei Cell Extracts Relies upon Sequence Microhomology Eukaryot. Cell, October 1, 2007; 6(10): 1773 - 1781. [Abstract] [Full Text] [PDF]
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R. L. Barnes and R. McCulloch Trypanosoma brucei homologous recombination is dependent on substrate length and homology, though displays a differential dependence on mismatch repair as substrate length decreases Nucleic Acids Res., May 11, 2007; 35(10): 3478 - 3493. [Abstract] [Full Text] [PDF]
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L. Glover, S. Alsford, C. Beattie, and D. Horn Deletion of a trypanosome telomere leads to loss of silencing and progressive loss of terminal DNA in the absence of cell cycle arrest Nucleic Acids Res., February 16, 2007; 35(3): 872 - 880. [Abstract] [Full Text] [PDF]
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C. Proudfoot and R. McCulloch Distinct roles for two RAD51-related genes in Trypanosoma brucei antigenic variation Nucleic Acids Res., December 2, 2005; 33(21): 6906 - 6919. [Abstract] [Full Text] [PDF]
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 B. Li, A. Espinal, and G. A. M. Cross Trypanosome Telomeres Are Protected by a Homologue of Mammalian TRF2 Mol. Cell. Biol., June 15, 2005; 25(12): 5011 - 5021. [Abstract] [Full Text] [PDF]
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 J. S. Bell and R. McCulloch Mismatch Repair Regulates Homologous Recombination, but Has Little Influence on Antigenic Variation, in Trypanosoma brucei J. Biol. Chem., November 14, 2003; 278(46): 45182 - 45188. [Abstract] [Full Text] [PDF]
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