Fig. 2. Bok-deficiency correlates with a lower proliferation rate and higher levels of DNA damage.

a, b Representative images and quantification of Ki67 staining. Data are reported as number of positive cells normalized to lesion area and analyzed by Kruskal–Wallis test (p < 0.0001, H(3) = 36.26). In panel (b), the p values from the post hoc analysis with Dunn´s correction are reported. c Live cell numbers evaluated as trypan blue exclusion over time. Data are presented as mean ± SEM and were analyzed by repeated measure two-way ANOVA (time, genotype, and interaction effects, p < 0.0001). Post hoc analysis with Bonferroni correction showed a significant difference between the genotypes at 72 h and 96 h (***p < 0.0001). d Cell cycle analysis performed with propidium Iodide (PI) staining. Data are presented as mean ± SEM and were analyzed by chi-square test (p = 0.0092, chi-square (2) = 9.373). e Quantification of γ-H2AX positive staining normalized to lesion area. Data were analyzed by Kruskal–Wallis test (p < 0.0001, H(3) = 22.34) and are reported in the figure as p values from the post hoc analysis with Dunn´s correction. For the quantification in panel (b) and (e), six lesions per slide/animal were evaluated and data are presented as dot plot and report mean ± SEM. For panel (c) and (d), each cell line was evaluated in at least three independent experiments.