Figure 2: ATM facilitates repair of TOP2-blocked DSBs.
From: ATM specifically mediates repair of double-strand breaks with blocked DNA ends
(a) Time course of γH2AX foci disappearance after 30 min 10 μM etoposide treatment and repair at different times following drug removal in Tdp2+/+ Atm+/+, Tdp2+/+ Atm−/−, Tdp2−/− Atm+/+ and Tdp2−/− Atm−/− confluency-arrested primary MEFs. Representative images of γH2AX foci (green) and DAPI counterstain (blue) for the 24 h repair time point are shown. Scale bar, 10 μm. (b) As above, in Tdp2+/+ and Tdp2−/− confluency-arrested primary MEFs with or without 10 μM ATM inhibitor (KU55933). (c) As above, in confluency-arrested primary fibroblast derived from A-T patients (AT) and wild-type controls (BJ1) depleted (shTDP2) or not for TDP2. In this case 20 μM etoposide treatment was applied. In all cases, average±s.e.m. of the percentage of foci remaining from at least three independent experiments and the minimal statistical significance between cells deficient in both TDP2 and ATM and all other cells by two-way ANOVA test with Bonferroni post-test is shown (*P≤0.05; **P≤0.01; ***P≤0.001).
