A novel paternal effect based on nicotine exposure reveals that offspring exhibit an adaptive, yet nonspecific, resistance to multiple toxins.

Epigenomic and transcriptomic analysis reveals that paternal obesity influences sperm histone H3 lysine 4 tri-methylation enrichment and placenta gene expression, which in turn negatively impact its development and function in a manner that may contribute to metabolic disease in offspring.

Exposing male mice to nicotine or cocaine enables their male offspring to cope with high doses of either, which suggests that such paternal effects are generic, rather than being a response to a specific type of stress.

Analysis of a spermiogenesis protein reveals a new chromatin requirement for synchrony between maternal DNA packaged in the egg and sperm-packaged paternal DNA in the first embryonic mitosis in Drosophila melanogaster.

The PVN-mPFC OT circuit is an important target for the treatment of disorders related to early adverse experiences.

A subset of genes in the mouse brain show dynamically regulated and unequal expression of maternally and paternally derived variants, with implications for brain development and function.

Adopted individuals in large-scale population based cohorts can be leveraged to partition maternal genetic effects into prenatal and postnatal components, helping elucidate the underlying mechanisms behind these associations, and for diseases, yielding important information regarding the optimal timing of interventions.

Rates of germline mutation accumulation are highly variable across families of similar genetic ancestry, and post-zygotic mosaicism is a substantial source of de novo mutations.

It is unclear how much a child's BMI at age 8 affects their depressive and ADHD symptoms after family-level factors are accounted for, but a substantial impact on anxiety symptoms is unlikely.