Abstract
For more than 40 years, multiple laboratories have studied Drosophila stocks that have been forced to evolve slowed rates of aging and increased average longevities. These stocks have been used to test both physiological and genetic theories of aging, yielding a number of interesting findings. A little-noticed problem is that these tests have too frequently produced positive results with respect to physiological and genetic mechanisms underlying slowed aging. A genomic interpretation of this copious success is that hundreds of genetic loci have undergone changes in allele frequency or gene expression as a result of selection for slowed aging. This implicates many genetic mechanisms in the control of aging, in general, across the diversity of aging species. As the technology for surveying genomes and transcriptomes continues to improve rapidly, the loci of aging are becoming ever easier to identify. But interpreting the detailed functional consequences of all of these loci presents a radically larger challenge. Like Croesus, experimental gerontology is faced with the problem of genomic foundations for aging which are extremely rich.
