Abstract

As cells age, their mitochondrial functions decline. Previous work from our lab showed that fast growing cells tend to lose mitochondrial DNA (mtDNA) and that this is caused by genetic variation in both nuclear and mitochondrial DNAs. We hypothesize that the cells that are genetically conditioned to grow fast will also age faster, and that this will be driven by interactions between mitochondrial and nuclear genomes. To test this, we are conducting chronological aging assays on yeast strains with high and low growth rates to look for correlations. We are also expanding a genomics resource in yeast that will allow us to map the genetic basis behind aging. Our ultimate goal is to gain a deeper understanding of the underlying genetic mechanisms of aging and the complex interplay between mitochondrial and nuclear genomes.