Meeting Abstract
In recent decades, ecologists and evolutionary biologists have investigated how various environmental challenges might lead to oxidative stress to evaluate the contribution of these stressors to aging processes. There is mounting evidence, however, that oxidative stress may play only a minor role in the decline in mitochondrial performance that is a hallmark of aging. Instead, there is a growing consensus in biomedicine that replication error, and not oxidative damage, is the source of most of the mitochondrial DNA (mtDNA) mutations that accumulate with aging. Replication error is a product of the process of making copies of mtDNA, where errors in copying and editing increase with the number of replication events. The processes responsible for mtDNA copying, editing, and those that alter the rate of replication are all subject to evolution by natural selection. Consequently, senescence via replication error may evolve within the context of the life history of a taxon. Given that different processes will contribute to variation in replication error and oxidative stress, it is critical that ecologists and evolutionary biologists begin to explicitly consider replication error in their measurements of the effects of and in their interpretations of the outcomes of environmental challenges. We will review those processes that alter mitochondrial performance with aging, discuss evidence that replication error is a crucial determinate of mitochondrial decline, and describe methods that can be used as indicators of replication error. And finally, we will discuss the role of that mitonuclear coadaptation plays in these processes.
