Genes & Development 26: 2690–2695 (2012)
In the above-mentioned article, the authors discovered that their sorting of genes showing noncanonical Ser2 phosphorylation was inverted. Genes denoted as “Very High FUS” in Supplemental Figure 4 should have been “Low FUS,” and genes denoted as “Low FUS” should have been “Very High FUS.” After this correction, both the canonical and noncanonical Ser2 phosphorylated genes show an increase in Ser2 phosphorylated RNAP2 around the transcription start site upon FUS knockdown, in support of our model. Figure 2B (below) and Supplemental Figure 4 (see Revised Supplemental Fig. 4 online) have been updated to reflect these corrected data. Also, on page 2691, right-hand column, this single sentence “These noncanonical genes also responded to the loss of FUS by undergoing a large increase in the levels of Ser2P near the TSS (Fig. 2B; Supplemental Fig. 4)” should replace these two sentences: “For these noncanonical genes, those with the least FUS bound to the TSSs had the highest average levels of Ser2P at their TSSs (Fig. 2B; Supplemental Fig. 4). Because this observation does not involve any siRNA knockdown, it provides further support that Ser2P levels are regulated by the presence of FUS.” All other next-generation sequencing data sets have been independently reanalyzed and validated.
This correction does not change the main conclusions of the article, which is that FUS binds the CTD of RNA polymerase II and regulates its phosphorylation at Ser2.
