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Fig. 2 | Genome Biology

Fig. 2

From: Cis-acting lnc-eRNA SEELA directly binds histone H4 to promote histone recognition and leukemia progression

Fig. 2

Lnc-eRNA SEELA binds histone components to activate target genes in cis. a The expression level of SERINC2 was significantly upregulated in patients with MLL leukemia (n = 26) compared with MLL-wt (n = 75) patients (Mann-Whitney test, **, P < 0.01). The expression level was calculated using 2-ΔCT method and was normalized to GAPDH. b Positive correlation of SERINC2 with SEELA was observed in patient samples (n = 101). Spearman analysis was used, and r = 0.44, P < 0.001 (upper) and r = 0.36, P < 0.001 (bottom). c qPCR showed that the mRNA levels of SERINC2 were decreased after knocking down SEELA. Error bars reflect ±SD (**P < 0.01; ***P < 0.001) in three independent experiments. d A schematic diagram shows the SEELA sites within their loci targeted by sgRNAs of the CRISPR-VPR activation system (upper). qPCR showed that the mRNA levels of SERINC2 and SEELA were significantly upregulated (bottom). Error bars reflect ±SD (**P < 0.01; ***P < 0.001) in three independent experiments. e The SEELA was enriched in the chromatin fraction of MV4-11 cells. The relative concentration was adjusted according to the chromatin concentration of positive control NEAT1. MALAT1 was another positive control and GAPDH was negative control. Error bars reflect ± SD in three independent experiments. f ChIP-qPCR showed the decreased POL II binding to the SERINC2 promoter after knocking down SEELA. Error bars reflect ±SEM (*P < 0.05) in three independent experiments. An IgG antibody was used as a negative control. g RIP-qPCR detection was used to assess the association of histone components with SEELA in MV4-11 and RS4;11 cells. Error bars reflect ± SEM in three independent experiments. An IgG antibody acted as a negative control. h, i Immunoblot detection of H3, and H4 retrieved by in vitro-transcribed tRSA-tagged SEELA sections from MV4-11 cell lysates. SEELA1 (SEELA1-V1/2/3) and SEELA2 (SEELA2-V1/2) presented significant enrichment. TRSA and beta-tubulin were used as negative controls. j A schematic diagram shows that upregulated lnc-eRNA SEELA acted in cis to activate SERINC2 transcription via binding with histone components

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