Fig. 7

Lasting alcohol-induced alterations in H3K4 me3, H3K9 ac, H3K9 me2, and H3K27 me3 within the prenatal cortex arising from an early gestational exposure. Pregnant dams were injected with 2.9 g/kg EtOH at GD7 and embryos harvested at GD17. Embryos were scored for ocular and cortical patterning defects, and sorted into three groups—control, EtOH exposed—morphologically normal, and EtOH exposed—malformed. After dissection of the fetal cortex, ChIP-qPCR analysis was performed on cellular extracts using antibodies recognizing H3K4 me3, H3K9 ac, H3K9 me2, and H3K27me3. a, c Heat maps representing fold change in the levels of the indicated post-translational modifications relative to samples derived from saline-exposed controls. In the experiments examining H3K4 me3 and H3K27 me3, four ChIP experiments were performed on a total of 15 brains across 5 different litters. For analysis of H3K9 ac and H3K9 me2, three ChIP experiments were performed on a total of 10 brains across 5 different litters. Two replicates of qPCR were performed on each ChIP. Significance was determined using a two-way ANOVA. Error bars represent SEM.*p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001. b, d Representative graphs depicting alcohol-induced alterations in chromatin structure. A complete analysis of individual genes may be viewed in Additional file 2