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. 2020 Nov 3;21:269. doi: 10.1186/s13059-020-02186-x

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© The Author(s) 2020

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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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