SKN-1 directly regulates target genes during the UPR.

<p>(A–L) ER stress-induced SKN-1 recruitment and transcriptional activation was analyzed at the SKN-1-regulated genes <i>pcp-2</i> (A–D), <i>atf-5</i> (E–H), and <i>gst-4</i> (I–L). TM treatment leads to SKN-1 recruitment (A, E, I), accumulation of Pol II that is phosphorylated at CTD Ser 2 (P-Ser2) (B, F, J), decreased Histone H3 occupancy (C, G, K), and increased H3-AcK56 density (D, H, L) at the site of transcription. Maps mark qPCR amplicons relative to the predicted transcription start site, with exons marked as black boxes. % ChIP signal is relative to input, and normalized to the highest signal for each run <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1003701#pgen.1003701-GloverCutter1" target="_blank">[44]</a>. In (D, H, L), a ratio of acetyl histone to histone signal is presented. For ChIP experiments in this study error bars represent SEM, and * p≤.05, ** p≤.01, *** p≤.001, relative to <i>pL4440</i> Control calculated using one-sided student's t-test. See also <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1003701#pgen.1003701.s002" target="_blank">Figure S2</a>.