Author Contributions S.J. and C.L.K. designed and coordinated analysis of single-cell data. S.J. and A.B.-C. performed the majority of the scRNA-seq analyses and visualizations. J.M. and G.B. contributed to the CNA analysis. Y.H. contributed to the algorithm for marker gene discovery. F.M.G.C., M.C., A.B.-C. and S.J. analyzed transcription factor activity in the scRNA-seq data. N.D.J., S.H. and S.J. contributed to the analysis of the bulk RNA-seq data and the data availability submission. M.V. contributed to timed mating and tissue isolation in developing mouse embryos. D.F., M.V. and L.K.D. and contributed to primary tissue isolation, preparation and production of scRNA-seq libraries. B.K. performed all experiments in cellular models. L.G., S.J., W.T.F. and K.K.M. contributed to literature review and cell cluster annotations. L.G. provided expert advice on identification of developing pre-cerebellar populations. M.K.M. and L.G.M. contributed to the clinical annotation of tumor samples. P.-E.L. and G.T. provided bulk adult human brain RNA-seq samples. M.R., B.P. and A.A. provided human fetal brain samples.

Childhood maltreatment (CM) has estimated prevalence among Western societies between 10% and 15%. As CM associates with increased risk of several psychiatric disorders, early age of illness onset, increased comorbidity and negative clinical outcome, it imposes a major public health, social and economic impact. Although the clinical consequences of CM are well characterized, a major challenge remains to understand how negative early-life events can affect brain function over extended periods of time. We review here both animal and human studies indicating that the epigenetic mechanism of DNA methylation is a crucial mediator of early-life experiences, thereby maintaining life-long neurobiological sequelae of CM, and strongly determining psychopathological risk.