In the oxidative stress hypothesis of aging therandom accumulation of oxidative damage over time ispostulated to cause aging. The pace at whichoxidative damage accrues determines the rate of aging,but it is less clear how the accumulation of randomdamage could cause the stereotypic pattern of aging. It has been proposed that oxidative damage induceschanges in gene expression, translating a random inputof damage into a patterned output. In support of thiswe show that in adult Drosophila melanogaster,with a deficiency in the anti-oxidant enzyme Cu, Znsuperoxide dismutase (Sod), an increase in oxidativestress, and a shortened life span, there isacceleration in the normal age-related temporalpattern of wingless gene expression. Theacceleration in the temporal pattern of winglessgene expression is proportional to the shortened lifespan suggesting that the shortened life span of Soddeficient animals is due, not to an abnormalpathological process, but to an increase in the rateof aging.