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. Author manuscript; available in PMC: 2018 Sep 15.
Published in final edited form as: Nat Microbiol. 2017 Nov 6;3(1):108–120. doi: 10.1038/s41564-017-0056-8

Figure 5. Reprograming of cellular m6A/m epitranscriptome during KSHV lytic replication.

Figure 5

a, Venn diagram comparing the number of methylated cellular genes before (latent) and after induction for lytic replication in KiSLK (left) and BCBL1-R (right) cells. b, Comparison of methylated cellular genes between KiSLK and BCBL1-R cells during latency (left) and lytic replication (right) at 48 h after induction. c, Most significant motifs in cellular m6A/m peaks identified by MEME in latent and lytic KiSLK and BCBL1-R cells. The latent KiSLK motifs are the same as in Fig. 4b and are replicated in this panel for ease of comparison. d, Distribution of cellular m6A/m peaks on transcripts in latent vs lytic cells in KiSLK cells (left) and BCBL1-R cells (right) as plotted by the Guitar software package. e, Comparison of significantly enriched pathways of cellular genes that are hypermethylated (left) or hypomethylated (right) as a result of reactivation from latency in KiSLK and BCBL1-R cells. f, Heat map of conserved hypermethylated pathways between KiSLK and BCBL1-R cells sorted by P-value. g, Heat map of conserved hypomethylated pathways between KiSLK and BCBL1-R cells sorted by P-value. h, The proportions of m6A and m6Am methylated transcripts, and the percentages of hypermethylated and hypomethylated genes. The results are from three biological replicates.