Using the MEP, we have discovered a distinct age-associated LOH phenotype in cells that retain respiration competence. This new LOH phenotype is distinguished by an apparent specificity for the rDNA array and dependence on the replication fork-block protein Fob1. As cells pass their median life span, they experience a significant increase in homologous recombination within the rDNA array which leads to LOH along a ∼875 kbp span from the rDNA to the telomere of the right arm of chromosome XII. These genomic alterations are mechanistically equivalent to events that generate partial uniparental disomy in mammalian cells, which has recently been found to occur at high frequency in many human cancers [6], [47]–[48].
