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Mol Biochem Parasitol. 2006 Feb;145(2):245-53. Epub 2005 Oct 26.

Trypanosoma brucei DMC1 does not act in DNA recombination, repair or antigenic variation in bloodstream stage cells.

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1
The Wellcome Centre for Molecular Parasitology, University of Glasgow, Anderson College, 56 Dumbarton Road, Glasgow G11 6NU, UK.

Abstract

Homologous recombination acts in the repair of cellular DNA damage and can generate genetic variation. Some of this variation provides a discrete purpose in the cell, although it can also be genome-wide and contribute to longer-term natural selection. In Trypanosoma brucei, a eukaryotic parasite responsible for sleeping sickness disease in sub-Saharan Africa, homologous recombination acts to catalyse antigenic variation, an immune evasion strategy involving switches in variant surface glycoprotein. In addition, T. brucei can undergo genetic exchange by homologous recombination in the tsetse vector, and some evidence suggests that this occurs by meiosis. Here, we show that T. brucei, Trypanosoma cruzi and Leishmania major each contain a single copy gene whose product is highly related to the eukaryotic meiosis-specific protein Dmc1, which is structurally and functionally related to Rad51. We show that T. brucei DMC1 is transcribed in the bloodstream stage of the parasite, where the gene can be mutated by reverse genetic disruption. DMC1 mutation does not, however, result in detectable alterations in DNA repair, recombination or antigenic variation efficiency in this life cycle stage.

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