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Fig. 8 | Genome Biology

Fig. 8

From: ARMC5 controls the degradation of most Pol II subunits, and ARMC5 mutation increases neural tube defect risks in mice and humans

Fig. 8

POLR2A ChIP-seq analysis of KO and WT NPCs. ChIP-seq was conducted using three pairs of biological replicates of WT and KO NPCs. A Pol II peak distribution in different gene regions of a representative pair of KO and WT NPC samples. B Means (solid lines) ± SE (shadows) of normalized read counts (read counts per million mapped reads) in a metagene analysis for a genomic region from − 2 kb of TSS to + 2 kb of TES. C Heatmaps of counts per million reads based on data from a representative pair of KO and WT NPC samples. D Pol II peak distribution (means ± SE) in a fixed region from − 10 kb upstream to + 10 kb downstream of TSS. E POLR2A read count tracks in the genes of Cdkn1a, Gadd45b, Mafa, and Pcdh8. The tracks were normalized so that each value was proportional to the read count per base pair per 10 million reads. F Upregulated mRNA levels of the four genes with elevated Pol II peak density in their genes according to RT-qPCR. The number of repetitions is indicated. *p < 0.05; ***p < 0.001 (paired two-way Student’s t tests). G Pausing indices (PI) of genes with detectable signaling in ChIP-seq. The proportions of genes with different PI are plotted. Solid lines: WT NPC samples; dashed lines: KO NPC samples. No statistically significant difference in PIs between the KO versus WT NPC samples for all the genes with ChIP-seq signals was found (paired two-way Student’s t tests followed by multiple-testing correction)

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