Fig 1: CRTC2 promotes NHEJ repair in vitro and in vivo.a Schematic diagram of I-SceI-induced NHEJ repair in EJ5-GFP U2OS cells. b NHEJ repair efficiency (left) in response to CRTC2 overexpression, and western blot analysis of I-SceI and CRTC2 expression (right) in EJ5-GFP U2OS cells (n = 3 biologically independent experiments). c NHEJ repair efficiency (left) in response to CRTC2 knockdown, and western blot analysis of I-SceI and CRTC2 expression (right) in EJ5-GFP U2OS cells (n = 3 biologically independent experiments). Immunofluorescence staining (d) and quantitative analysis (e) of 53BP1 foci formation at 0, 0.5, 2, 4, 8, and 12 h after IR (6 Gy) in control and CRTC2-knockout HCCLM3 cells (n = 40 cells per group). Scale bars, 10 µm. f Schematic diagram of VDJ rearrangement and primer locations in pro-B cells. g Pro-B cell sorting process with CD19, B220, IgM, and CD43 from spleen of Crtc2+/+ and Crtc2−/− mice (left) and mRNA level of distal and proximal VDJ rearrangement detection by qPCR (right) (n = 3 mice per group). h Schematic diagram of mouse immunoglobulin class switch recombination (CSR) in mature B cells. i Serum IgM, IgG1, IgG2a, IgG2b, IgG3, and IgA levels in Crtc2+/+ and Crtc2−/− mice (n = 10 mice per group). j Splenic B cells cultured under LPS or LPS/IL4 stimulation following CSR to IgG3 (left) and IgE (right) (n = 3 mice per group). All data are shown as the mean ± SEM. Comparisons between two groups were analyzed by Student’s t test. Comparisons between three or more groups with two or more conditions were assessed by two-way ANOVA. All statistical tests were conducted as two-sided. Source Data are provided with this paper.