RES complex mutants show mild widespread intron mis-splicing.

<p><b>(A)</b> Biplot illustrating percent intron retention (PIR) in each of the RES mutants and the corresponding phenotypically wild type (WT) siblings. Blue and red dots correspond to introns with higher inclusion in the mutant and WT, respectively, using a cutoff of ∆PIR >15. Insets show exon gene expression levels in the same conditions (see <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1007473#pgen.1007473.s011" target="_blank">S4 Fig</a> for details). <b>(B)</b> Stacked barplot showing the number of mis-regulated events upon RES loss-of-function. Clearly, most changes are intron retention supporting the role of the RES complex in splicing. <b>(C)</b> Scheme showing how PIR was measured (adapted from Braunschweig et al. [<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1007473#pgen.1007473.ref022" target="_blank">22</a>]; see <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1007473#sec007" target="_blank">Methods</a> for details). <b>(D)</b> Euler diagram showing the number of retained introns (∆PIR>5) in the three mutants and the inter-mutant overlaps. <b>(E)</b> RNA-seq read density across the <i>rrp8</i> gene in <i>bud13</i>, <i>rbmx2</i> and <i>snip1</i> mutants and their corresponding phenotypically WT siblings. Intronic signal increases in RES mutants (∆PIR>15) (dark blue) (dotted square box). <b>(F)</b> RT-PCR assays validate the increased retention of an <i>rrp8</i> intron (from panel E) in <i>bud13</i>, <i>rbmx2</i> and <i>snip1</i> mutants compared to the corresponding phenotypically WT siblings.