Pubertal development is a significant transitional process for adolescence as they move into reproductive maturity. This transition may also come with significant negative health and psychosocial consequences, however. Because early puberty has been linked to an array of health-related issues, factors that predict pubertal development differences among adolescents has been the focus of considerable research. One family factor that has been reliably linked to pubertal development, particularly girls' age at menarche (AAM), is father absence. Whether father absence causes differences in AAM is currently being debated by researchers. On one hand, some research suggests that father absence is an environmental influence that causally regulates AAM. On the other hand, some research suggests that the association is due to genetics: Genetic factors that might dispose a father to be absent are passed down to their daughters, which may dispose them to earlier AAM. This research is limited, however, in that both perspectives take a genes versus (or plus) environment approach, which overlooks how genes and environments operate together. The purpose of this proposal is to examine gene-environment interactions and epigenetic mechanisms of the relation between father absence, pubertal development, and related risky sexual behaviors in adolescent boys and girls.