Fig. 2
Sotos syndrome accelerates epigenetic aging. a Screening for epigenetic age acceleration (EAA) in developmental disorders. The upper panel shows the p values derived from comparing the EAA distributions for the samples in a given developmental disorder and the control (two-sided Wilcoxon’s test). The dashed green line displays the significance level of α = 0.01 after Bonferroni correction. The bars above the green line reach statistical significance. The lower panel displays the actual EAA distributions, which allows assessing the direction of the EAA (positive or negative). In red: EAA model with cell composition correction (CCC). In blue: EAA model without CCC. ASD, autism spectrum disorder; ATR-X, alpha thalassemia/mental retardation X-linked syndrome; FXS, fragile X syndrome. b Scatterplot showing the relation between epigenetic age (DNAmAge) according to Horvath’s model [8] and chronological age of the samples for Sotos (orange) and control (gray). Each sample is represented by one point. The black dashed line represents the diagonal to aid visualization. c Scatterplot showing the relation between the epigenetic age acceleration (EAA) and chronological age of the samples for Sotos (orange) and control (gray). Each sample is represented by one point. The yellow line represents the linear model EAA ~ Age, with the standard error shown in the light yellow shade. d Scatterplot showing the relation between the score for the epigenetic mitotic clock (pcgtAge) [39] and chronological age of the samples for Sotos (orange) and control (gray). Each sample is represented by one point. A higher value of pcgtAge is associated with a higher number of cell divisions in the tissue. e Scatterplot showing the relation between the epigenetic mitotic clock (pcgtAge) acceleration and chronological age of the samples for Sotos (orange) and control (gray). Each sample is represented by one point. The yellow line represents the linear model pcgtAgeacceleration ~ Age, with the standard error shown in the light yellow shade