We hypothesize that the aging process may involve attenuation of an activity that normally keeps the rate of homologous recombination relatively low within the rDNA array. By extension, elimination (e.g. by gene mutation) of such an activity in young cells should phenocopy the age-associated increase in LOH. Our characterization of the age-associated LOH phenotype has delineated two criteria such candidate activities must possess: Deletion of a candidate activity must show a FOB1-dependent increase in LOH at the MET15 locus, and the ratio of reciprocal-to-nonreciprocal LOH events should be the same as in wild type cells.
