Fig. 2

Lrrk2-deficiency disturbs genomic stability and epigenetic modification during aging. a The expression levels of γH2A.X and H3K9me2 were detected by western blot analysis from the striatal samples of Lrrk2^+/+ and Lrrk2^−/− mice at 2, 12 and 24 months of age. b, c The ratios of γH2A.X (b) and H3K9me2 (c) against H2A and H3, respectively. N = 3 per genotype and per time point. Data were presented as mean ± SEM. 2way ANOVA analysis with Sidak’s multiple comparisons test of γH2A.X, ^****p < 0.0001 (Lrrk2^+/+ vs. Lrrk2^−/− at 12 months of age), ^****p < 0.0001 (Lrrk2^+/+ vs. Lrrk2^−/− at 24 months of age). 2way ANOVA analysis with Sidak’s multiple comparisons test of H3K9me2 expressions, ^****p < 0.0001. d Co-staining of γH2A.X and CTIP2 in the striatal sections of 2-, 12-, and 24-month-old Lrrk2^+/+ and Lrrk2^−/− mice. Scale bar, 5 μm. e The ratios of SPNs with 10 or more γH2A.X-positive foci in the nuclei. N = 3 or 4 mice per genotype, 400 neurons per animal. Data were presented as mean ± SEM. Unpaired t-test, ^*p = 0.0126 (12 M, +/+ vs. −/−), ^*p = 0.0132 (24 M, +/+ vs. −/−)