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. 2016 Nov 28;45(3):1219–1232. doi: 10.1093/nar/gkw1170

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© The Author(s) 2016. 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-nc/4.0/), which permits non-commercial re-use, 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 3. — MLH1 deficiency-induced TSI is elevated by etoposide and is abolished by ATM or ATR inhibition. HeLa expressing shMLH1 or control shLUC, HCT116, and HCT116^MLH1 were treated with or without etoposide (3 μM) for 2 h and recovered for 24 h after drug removal. Metaphase cells from drug treated and untreated samples were analyzed by telomere FISH. (A) Frequency of TSI measured in HeLa expressing shLUC and shMLH1 following etoposide treatment. (B) Frequency of TSI measured in HCT116 cells and HCT116^MLH1 following etoposide treatment. (C) Percentage of TSI events on a single sister chromatid (single insertion) versus TSI events on two sister chromatids (double insertion) following etoposide treatment. (D) Frequency of TSI measured in HeLa-shLUC and HeLa-shMLH1-1 treated with 10 μM ATM inhibitor (ATMi) or 10 μM ATR inhibitor (ATRi). In each experiment, >1500 chromosomes from each sample were analyzed and each experiment was repeated with three independent replicates.