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Fig. 4 | Genome Biology

Fig. 4

From: APC mutations dysregulate alternative polyadenylation in cancer

Fig. 4

APC binds mRNAs proximal to poly(A) signal sequences. A Overview of computational pipeline, including mapping of HITS-CLIP data and detection of enriched binding sites using DEWseq, definition of a 1000-bp widnow surrounding identified binding sites, and quantification of distance to the nearest canonical poly(A) signal sequences (AATAAA or ATTAAA). B Density plot of nearest canonical poly(A) sequence from identified APC binding sites using HITS-CLIP. Dotted lines indicate a 50-bp window of identified HITS-CLIP binding. Maximal signal occurring at + 62.19 bp from the center of APC binding. C Representative read coverage plots of APC HITS-CLIP binding data. Plots illustrate two of the most-enriched genes, Sox11 and Rab23, identified from reanalysis of the APC HITS-CLIP binding data from Preitner et al. (2014) [26]. D Violin plots of distance from APC binding site to high-confidence poly(A) sites from PolyADB v3 [32]. Poly(A) sites are binned into either proximal (most 5′ poly(A) signal within the 3′ UTR), distal (most 3′ poly(A) signal within the 3′ UTR), or intermediate (all other poly(A) sites). P values from a two-sided Wilcoxon rank-sum test. E Boxplot comparing the differences in change of 3′ UTR length between colorectal adenocarcinoma samples with or without APC loss-of-function mutations for genes identified as direct binding targets of APC from Pretiner et al. (2014) (blue) or genes not identified in their experiments (white). A more positive value indicates, on average, a longer 3′ UTR in the APC loss-of-function colorectal adenocarcinoma samples. P value from a two-sided Wilcoxon rank-sum test

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