Prenatal and postnatal effects of gestational immune activation on synaptic and neurodevelopmental pathways via epigenetic mechanisms (ChIP-seq)

Previous epidemiological research suggests that maternal immune activation (MIA) during early pregnancy is a significant risk factor for neurodevelopmental and psychiatric disorders in offspring. Epigenetic factors and chromatin-related phenomena remain largely plastic during the course of prenatal and early postnatal development, allowing a dynamic impact of environmental effects on access to genes and regulatory elements. In this study, we tested the effects of maternal infection with the mouse-adapted influenza A/WSN/33 (H1N1) virus as a MIA model. Additionally, to assess the prenatal and postnatal effects of MIA, we cross-fostered half of the neonatal mice immediately after birth.This study includes RNA-seq and ChIP-seq profiling (H3K27ac, H3K4me3) from the prefrontal cortex of MIA-exposed and control mice. RNA-seq and ChIP-seq data are submitted under separate Series and linked via sample annotations.