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. 2020 Jun 15;9(6):60. doi: 10.1038/s41389-020-00244-4

Fig. 2. USP42 promotes HR by facilitating DNA-end resection.

Fig. 2

a U2OS cells transfected either with siRNA control (Ctrl) or siRNA targeting USP42 were treated with CPT or mock treated. Cell extracts were analysed by immunoblotting with the indicated antibodies. Asterisk indicates endogenous USP42. Immunoblotting with the anti-γH2AX antibody was used as a control for DNA damage induction. b A DNA-end resection assay was carried out with the cells transfected with the indicated siRNAs (mean ± SEM, n = 3). The siRNA targeting CtIP was a positive control. c RAD51 foci formation efficiency was examined with cells transfected with the indicated siRNAs (mean ± SEM, n = 3). The population of cells with >5 RAD51 foci was plotted. d Cells transfected with the indicated siRNAs were subjected to a clonogenic survival assay (mean ± SEM, n = 4 for siCtrl and siUSP42#2, n = 3 for siUSP42#1, siUSP42#3, and siXRCC4). The siRNA targeting XRCC4 was used as a positive control. e U2OS, USP42 KO, or USP42 KO cells complemented with either GFP or GFP-USP42 (FL) were treated with CPT and subjected to immunoblotting analysis with the indicated antibodies. End. USP42: endogenous USP42. f The indicated cell lines were subjected to a clonogenic survival assay [mean ± SEM, n = 6 for U2OS, USP42 KO + GFP and USP42 KO + GFP-USP42 (FL), n = 5 for USP42 KO]. ***p < 0.005.