Fig. 4: Prenatal e-cigarette exposure changed H3K4me1-H3K27me3 transition and bivalency in the genes involved in neuronal cell type specification. | Communications Biology

Fig. 4: Prenatal e-cigarette exposure changed H3K4me1-H3K27me3 transition and bivalency in the genes involved in neuronal cell type specification.

From: Single-cell profiling of H3K4me1-H3K27me3 revealed bivalent regulation of abnormal neuronal development caused by prenatal e-cigarette vaporing

Fig. 4

A Bar plot showing the number of differential histone peaks (5k bin) of H3K4me1 and H3K27me3 induced by prenatal e-cigarette exposure in each cell type. B Pie charts showing the distribution and localization of differential histone peaks of H3K4me1 (top) and H3K27me3 (bottom) in relation to genic regions. C Venn diagrams showing the number of genes with significantly differential methylation of H3K4me1 or/and H3K27me3 in excitatory neurons (top) or inhibitory neurons (bottom), respectively. Heatmaps showing the differential histone peaks (5k bin) of H3K4me1 (D) and H3K27me3 (E) in excitatory and inhibitory neurons, respectively. Histone mark signal was normalized to fragments per kilobase per million mapped reads (FPKM). Peak coverage plots showing the e-cig induced changes in H3K4me1 (F) and H3K27me3 (G) of three representative bivalent genes, Elavl2 (F), Celf2 (G), and Kcnc2 (H), in excitatory neurons and inhibitory neurons.

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