Fig. 2: TIAL1 crosslinks and binding to target mRNAs.

a Crosslinked Tial1 liver viP-CLIP reads harboring characteristic T-to-C conversions primarily map to the precursor mRNA and mRNA categories. b PARalyzer-based binding sites distribution in various RNA-species primarily indicates intronic and 3’UTR binding. c Normalized density distribution of Tial1 liver viP-CLIP binding sites (red line) over 3’UTRs compared to a randomized background (gray line). Tial1 binding accumulates close to the poly adenylation and cleave sites. Sequence logo for the RNA recognition element of Tial1 top 1000 3’UTR sequence read clusters is indicated in the graph. d Normalized density distribution of TIAL1 liver viP-CLIP binding sites (red line) over introns compared to a randomized background (gray line). An enrichment of TIAL1 binding at 5′ and 3′ splice sites is observed. Sequence logo for the RNA recognition element of Tial1 top 1000 intronic sequence read clusters is indicated in the graph. e Venn diagram with a target overlap of the two liver viP-CLIPs for the endogenous TIAL1 and Ad-Tial1 (n = 8 and n = 5 mice). f Venn diagram with an overlap of binding sites in 3’UTR for both replicates (n = 8 and n = 5 mice). g Scatterplot of normalized crosslinked read counts for overlapping targets of both replicates. Spearman correlation and statistics are depicted. h Scatterplot of T-to-C counts in crosslinked read per gene versus the expression value in FPKM. Spearman correlation and statistics are depicted. i Liver Tial1 viP-CLIP targets identified in the study. j Representative images of TIAL1 stainings in primary human hepatocytes treated with DMSO (vehicle control), AcLDL (120 µM), or Simvastatin (5 µM) for 24 h (n = 3). k Comparisons of cells treated for 46 h with statin (left) and 24 h with statin and then washed and cultured for additional 22 h without statin (n = 3). l TIAL1 immunoblot of the samples in (j) after nucleocytoplasmic fractionation (n = 2). Source data are provided as a Source Data file.