Aging starts at the cellular level and shares many commonalities with cancer such as increased cellular damage and impaired DNA repair. We are incorporating current methodologies of sorting young and old cells in the unicellular organism, S. cerevisiae, to address fundamental questions in the area of aging. The current project includes understanding the interplay between DNA damage accumulation and aging. We are asking the following questions: 1. Does DNA damage accumulation drive cellular aging? 2. Do cells that prematurely age have a molecular profile that resembles cells that naturally age 3. Do repair pathways become disrupted during aging? 4. Does nucleolar breakdown inhibit repair pathways leading to genome-wide DNA damage?