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. Author manuscript; available in PMC: 2021 Jun 16.
Published in final edited form as: Immunity. 2020 Jun 3;52(6):1007–1021.e8. doi: 10.1016/j.immuni.2020.05.003

Figure 4. OAS family genes are highly upregulated via epigenetic regulation in response to Mettl3 loss in HSPCs.

Figure 4.

(A) Oas family gene expression in vcMettl3+/+ and vcMettl3−/− E14.5 fetal liver LSK cells as measured by RNA-seq (n=3 biological replicates per group).

(B) Percentage of genes with annotated m6A peaks in Oas genes compared to the remaining genes upregulated in vcMettl3−/− LSK. The meta-analysis was performed with 52 different published m6A datasets.

(C) Number of genes with significantly increased (red) versus decreased (green) H3K4me3 occupancy around the transcription start site (TSS) in vcMettl3−/− versus vcMettl3+/+ LSK cells (n=2 biological replicates per group).

(D) Scatterplot comparing gene expression changes (y-axis) versus H3K4me3 occupancy changes (x-axis) between vcMettl3−/− and vcMettl3+/+ LSK cells. Genes with consistent and significant epigenetic and gene expression changes are highlighted (red=up, green=down).

(E) H3K4me3 occupancy profiles of Oas1g, Oas2 and Rag1 (3k bp around the TSS) in vcMettl3+/+ and vcMettl3−/− LSK cells. The average normalized signal and standard error from 2 replicates is displayed.

The P value in (B) was calculated using two-tailed Wilcoxon rank-sum test.

See also Table S1.