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. 2013 Feb 1;41(5):3173–3189. doi: 10.1093/nar/gkt051

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© The Author(s) 2013. Published by Oxford University Press.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 3. — The MRX complex plays a DSB independent role at RFBs (A) Shown are isogenic strains of mre11-H125N (LBy-623), GAL-FOB1 mre11-H125N (LBy-631). (B) Deletion of KU70 does not suppress the phenotype of GAL-FOB1 mre11 mutant. Shown are isogenic strains of GAL-FOB1 (LBy-413), GAL-FOB1 mre11Δ (LBy-756), GAL-FOB1 ku70Δ (LBy-905) and GAL-FOB1 mre11Δ ku70Δ (LBy-903). (C) Molecular bridging is required by MRX complexes is required at protein–DNA barriers. Shown are isogenic strains of GAL-FOB1 mre11Δ (LBy-756), rad50^sc (LBy-1061), GAL-FOB1 rad50^sc (LBy-1070), rad50^sc⁺^h (LBy-1062) and GAL-FOB1 rad50^sc⁺^h (LBy-1071) (D) Absence of Mre11 does not generate more DSBs in the rDNA, but abnormal structures are detected. Shown is a DSB assay for GAL-FOB1 (LBy-413), GAL-FOB1 mre11Δ (LBy-756) and GAL-FOB1 mre11Δ rad52Δ (LBy-680). Digested rDNA units (M), partial digested rDNA units (P), converging forks (CF), stalled forks at RFB (SF), replication independent DSBs (DSB), replication dependent DSB (rep DSB).