To confirm this result, we attempted to stabilize Sir2 protein levels by a second method. In a previous study, Dang, et al. found that deletion of SAS2, the gene encoding the catalytic histone acetyltransferase subunit of the SAS complex that acts antagonistically to Sir2 for modification of histone H4 at lysine 16, stabilized Sir2 levels in aging cells [36]. When we constructed a sas2 deletion strain in the MEP background and examined Sir2 protein levels, we saw no evidence of Sir2 stabilization in this mutant background (Figure 6C). Finally, we asked whether deletion of fob1, which does suppress age-associated rDNA recombination, might also stabilize Sir2 protein levels in aging cells. Again, we observed no stabilization of Sir2 protein levels (Figure 6C). Thus, we found no evidence of a correlation between Sir2 protein levels and LOH rates in aging populations.
