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. 2011 Aug 1;22(15):2741–2753. doi: 10.1091/mbc.E11-05-0426

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© 2011 Leung et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).

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FIGURE 3: — Loss of SIR function rescues the heat-sensitive phenotype of htbK123R and Δset1 cells. Dilutions 1:9 of yeast were plated on YPAD and grown for 3 d at either 30 or 37°C. Strains used here are WT (FGY8.2), htbK123R (FGY8.3), htbK123R Δsir4 (FGY8.11), Δsir4 (FGY8.10), Δsir2 (FGY8.12), htbK123R Δsir2 (FGY8.13), Δsir3 (FGY8.14), htbK123R Δsir3 (FGY8.15), Δset1 Δsir4 (FGY8.16), and Δset1 (FGY8.6). To analyze the effects of expressing a dominant-negative version of Sir4 (SIR4–CTERM), htbK123R cells (FGY8.3) carried a pVV214-based plasmid expressing the carboxy-terminal 167 residues of Sir4.