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. 2014 Feb 13;196(4):1029–1039. doi: 10.1534/genetics.113.158824

Figure 1.

Figure 1

The gas1 gcn5 double mutant is synthetically lethal. (A) Synthetic lethality of gas1 gcn5 is due to loss of catalytic activity of both Gas1 and Gcn5 and is not rescued by the osomoregulator sorbitol. Serial dilutions of wild type (LPY18050), gcn5 (LPY12264), gas1 (LPY18081), gas1 gcn5 (LPY16798), and gas1 gcn5 covered by plasmid-born p-gcn5-KQL (gcn5*; LPY16800) or p-gas1-E161Q, E262Q (gas1**; LPY16801) were plated on selective media with 5-FOA, to counterselect the p-GCN5, URA3 plasmid, with or without 1 M sorbitol at 30°. (B) Primary Gcn5-containing complexes are shown with color coding to highlight defined subunits in each functional module. Boldface type indicates subunits analyzed in this study (adapted from Lee et al. 2011). (C) gas1 has modest synthetic interactions with components of all three complexes tested, including increased temperature sensitivity with gas1 sgf73 and gas1 ahc1 at 37°. A more severe effect is observed in which gas1 rtg2 is synthetic sick at 30° and dead at 37°. Serial dilutions of wild type (LPY5), ada2 (LPY6439), gas1 (LPY10129), gas1 ada2 (LPY19197), sgf73 (LPY19816), gas1 sgf73 (LPY19771), spt20 (LPY16914), gas1 spt20 (LPY19630), ahc1 (LPY17370), ahc2 (LPY18518), gas1 ahc1 (LPY19467), gas1 ahc2 (LPY19414), rtg2 (LPY18206), and gas1 rtg2 (LPY18372) were plated on SC at either 30° or 37°. Here, and in other figures, gas1 and gcn5 refer to the null alleles, whereas the gas1 catalytic mutant (Carotti et al. 2004) is denoted as gas1** and the gcn5 catalytic mutant (Wang et al. 1998) as gcn5*.