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. 2012 Dec 7;41(2):943–960. doi: 10.1093/nar/gks1192

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© The Author(s) 2012. Published by Oxford University Press.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc/3.0/), which permits non-commercial reuse, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com.

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Figure 1. — Growth and repair efficiency of T. brucei BRCA2 mutants. (A) Locations of conserved domains are shown diagrammatically within the T. brucei BRCA2 polypeptide: BRC repeats (black boxes), and sub-domains of the DSS1-DNA binding region (grey boxes: H, helical domain; T, tower domain; 1, 2, 3, OB domains). (B) Growth is shown of WT, BRCA2 heterozygous (+/−) and brca2 homozygous (−/−) mutants cells in T. brucei Lister427 bloodstream form (427BSF) cells and in PCF cells from Lister427 (427PCF) and TREU927 (927PCF) strains. Cell densities were measured in vitro at 24 h intervals; bars indicate standard errors from three experiments. (C) EC₅₀ values of the same T. brucei BSF and PCF strains are shown, comparing WT, BRCA2+/− and brca2−/− cells exposed to phleomycin. EC₅₀ values are the mean from three experimental repetitions expressed as a percentage of WT; bars indicate standard error.