This thesis concerns the asymmetric mechanism by which the "molecular aging clock" is reset in the budding yeast Saccharomyces cerevisiae, which is of great interest considering that many organisms' cells--including human stem cells--undergo this process. When yeast divides, it ages a generation, while daughter cells begin life at generation zero. One theory surrounding this process in yeast is the extrachromosomal rDNA circle (ERC) aging theory. ERCs are generated spontaneously in mother cells as they age, and thus accumulate exponentially in older cells. Daughter cells from young mothers benefit from asymmetric aging, but as mothers age, they produce daughters that prematurely senesce. Studies suggested that ERCs may be a cytoplasmic senescence factor that is passed from mother to daughter as the mother ages, possibly due to the mother's inability to maintain cellular pathways responsible for asymmetric processes as she ages. ASH1 is a gene that encodes an asymmetrically-distributed protein that halts expression of HO endonuclease--an enzyme critical to mating-type switch--in daughter cells. Previous studies in our lab showed that deleting ASH1 led to a decrease in daughter lifespan compared to wild-type strains. In this thesis, I present evidence of a possible connection between ASH1 and cell cycle regulation. Furthermore, the detection of ERC accumulation via Southern blotting in the mutant ASH1 strain, but not the wild-type strain, provides support that ERCs may be a senescence factor in yeast. Lastly, preliminary microarray analysis reveals several genes related to cell cycle regulation being affected by the deletion of ASH1.