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. 2019 Jan 18;47(6):2966–2980. doi: 10.1093/nar/gkz009

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© The Author(s) 2019. Published by Oxford University Press on behalf of Nucleic Acids Research.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 3. — MRE11 is involved in cellular tolerance to CTNAs. (A) Cellular proliferation of MRE11^D20A/− mutant cells. They proliferate almost the same as wild-type cells. (B) Accumulation of RAD51 at DNA damage sites is indistinguishable between wild-type and MRE11^D20A/− mutant cells. Representative fluorescence microscopic images (upper panel) and quantification (lower panel) of Rad51 foci in the indicated cell lines before and 1 h after irradiation of 2 Gy IR. Statistical analysis was done by Student's t-test (n.s.: not significant). (C–F) Clonogenic cell survival to the indicated agents was analyzed as described in Figure 1A.