Correction to: Nature Cell Biology https://doi.org/10.1038/ncb3598, published online 28 August 2017.
In the version of this Article originally published, Supplementary Fig. 6j showed incorrect values for the LS and AG4 glutathione samples, and Fig. 5c and Supplementary Fig. 6j did not include all n = 6 samples for the hESC, Y-hiPSC and AG4-ZSCAN10 groups as was stated in the legend. In addition, the bars for hESC, Y-hiPSC, AG4-ZCNAN10, AG4 and LS in Supplementary Fig. 6i and j have been reproduced from Fig. 5b and c, respectively. Figure 6e was also reproduced in the lower panel of Supplementary Fig. 6h, to enable direct comparison of the data, however this was not explained in the original figure legends. The correct versions of these figures and their legends are shown below, and Supplementary Table 5 has been updated with the source data for all numerical data in the manuscript.
Corrected Fig . 6 legend:
Impaired DNA damage response in human A-hiPSCs caused by deregulation of ZSCAN10 and GSS and recovered by ZSCAN10 expression. a, Excessive oxidation capacity with elevated glutathione in A-hiPSCs, and recovery by ZSCAN10 expression. The total glutathione level was measured to determine the maximum oxidation capacity. Excessive oxidation capacity of glutathione in A-hiPSCs is normalized to the level of hESCs and Y- hiPSCs by transient expression of ZSCAN10. Glutathione analysis was conducted with the glutathione fluorometric assay. Mean ± s.d. is plotted for three biological replicates with two independent clones (n = 6) in each sample group from each condition. Statistical significance was determined by two-sided t-test. b, ROS scavenging activity of hESCs, Y-hiPSCs, A-hiPSCs and A-hiPSCs–ZSCAN10. A cellular ROS assay kit (DCFDA assay) was used to measure H2O2 scavenging activity. A-hiPSCs show strong H2O2 scavenging activity, with a reduced response against treatment with TBHP (tert-butyl hydrogen peroxide; stable chemical form of H2O2, 3 h); the response is recovered by ZSCAN10 expression. Mean ± s.d. is plotted for four biological replicates in each sample group from each condition (n = 4). Statistical significance was determined by two-sided t-test. c, Immunoblot of pATM showing recovery of the DNA damage response after phleomycin treatment in three independent clones of A-hiPSCs with shRNA-mediated knockdown of GSS. d, Immunoblot of pATM showing that lentiviral expression of GSS cDNA impairs the DNA damage response in three independent clones of Y-hiPSCs after phleomycin treatment. e–g, Copy-number profiling analysis of human iPSCs43. Schematic diagrams represent seven rearranged A-hiPSCs, four non-rearranged A-hiPSCs and five non-rearranged A-hiPSCs– ZSCAN10 in the genetically controlled setting of A-hiPSCs. Ten non-rearranged Y-hiPSCs, which were generated from a different tissue donor, were also included. A-hiPSCs (n = 11 (7/11), P = 0.64), (These data are also presented in Supplementary Fig. 6h), A-hiPSCs–ZSCAN10 (n = 5 (0/5), P* = 6.3 × 10−3) and Y-hiPSCs (n = 10 (0/10), P* < 4 × 10−5). The number in parentheses represents detected rearrangements and P and P* are the observed and estimated likelihoods of detecting no rearrangements in the absence of lineage effects using a binomial distribution, respectively50. Unprocessed original scans of blots are shown in Supplementary Fig. 7.