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The Dynamics of Genome Organization and Expression during the Aging Process

Aging may be explained, to some extent, as a stochastic process of macromolecular damage. The rate of such a process should then determine longevity and be genetically controlled, as can be derived from the species specificity of maximum life span. Alterations in the genomic organization and expression could be a major driving force behind age-related deterioration and death. Indeed, somatic mutational theories of aging have been formulated more than 30 years ago.'.* However, the role, if any, of somatic instabilities in the etiology of aging and agerelated disease has not yet been revealed. In order to properly investigate this hypothesis, four aspects should be studied for each species and each cell and tissue type separately: (1) the frequency at which somatic mutations occur spontaneously; (2) the type of mutations and their location in the genome; (3) the effect of mutations on (the regulation of) gene expression; and (4) the relation of spontaneous mutagenesis to the rate of the aging process and to the pattern of age-related pathology. Here we will briefly review the presently available data concerning these aspects, with special emphasis on the use of advanced technology to study low-frequency DNA changes in different organs and tissues of aging animals.