An integrative omics approach reveals posttranscriptional mechanisms underlying circadian temperature compensation

We apply 3'-End-RNA-seq based sequencing to globally quantify polyadenylation sites and transcript isoform abundance in human U-2 OS cells under wild-type and CPSF6 knock-down conditions at 3 different temperatures (32°C, 37°C and 39°C). We show that CPSF6 knock-down as well as temperature alterations lead to global changes in 3' UTR length and transcript abundance. By means of a differential response analysis with respect to temperature changes in wild type and temperature-decompensated CPSF6 knockdown cells, we reveal candidate genes underlying circadian temperature compensation. Overall design: Global changes in 3' UTR length and transcript abundance upon CPSF6 knockdown and temperature alterations.