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. 2020 Sep 8;11:4455. doi: 10.1038/s41467-020-18259-1

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© The Author(s) 2020

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — a The fCLIP target transcripts were classified as strong-, median- or weak-affinity with MTA1 according to the fCLIP-seq data normalized by the RNA-seq expressional abundance in the control. The empirical cumulative distribution function of the log2 CrMTA1/control fold changes of the abundance for each set were plotted. b Hierarchical clustering heatmap of the differentially expressed genes (DEGs) between CrMTA1 and the control. c Venn diagram showing the overlap between the MTA1 binding transcripts (fCLIP genes) and DEGs. d The ChIP promoters were classified as strong-, median- or weak-affinity with MTA1. The affinity was defined using a binding affinity score, which is the sum of fold enrichment (MTA1-ChIP/Input) of peaks in the gene promoter region according to the ChIP-seq data. The empirical cumulative distribution function of the log2 CrMTA1/control fold changes of the abundance for each set were plotted. e Venn diagram showing the overlap between the MTA1 binding gene promoters (ChIP-promoters) and DEGs. f The fCLIP target transcripts were classified as strong-, median- or weak-affinity with MTA1 according to the fCLIP-seq data normalized by the RNA-seq expressional abundance in the control, and the empirical cumulative distribution function of the log2 CrMTA1/control fold changes of the AS ratio for each set were plotted. g The ChIP promoters were classified as strong-, median- or weak-affinity with MTA1, and the empirical cumulative distribution function of the log2 CrMTA1/control fold changes of the AS ratio for each set were plotted. h Bar plot showing that MTA1 deletion generated more IR events. IntronR, intron retentions; ES, exon skips; MXE, mutually exclusive exons; A5SS, alternative 5’ss; A3SS, alternative 3’ss. i Venn diagram showing that the transcripts of most of the RASGs were bound by MTA1. j RT-qPCR validation for the non-IR and IR events. Data are represented as mean ± SD (n = 3 per group). a, d, f and g One-way ANOVA with Tukey’s multiple comparisons test. h Two-tailed Fisher’s exact test. j Two-tailed Student’s t-test.