Most studies of aging are conducted in humans and domestic or laboratory animals, i.e. in conditions where artificial environment protection is applied, This yields changes in physiology and behavior, which set up organism's state unobserved in wild life. This state may be less adequate to the evolutionary adjusted genetic construction of an organism, which generates a hypothesis that in natural niches the aging rate can be lower and stress resistance can be higher than in captivity despite the fact that life expectancy in habitat is essentially lower than that in laboratory conditions due to high external mortality. Direct test of this hypothesis is difficult because of problems related to reconstruction of natural environment conditions in the laboratory. Substantial life-extending effect of some mutated genes can serve as indirect test of the hypothesis. We propose that in some cases genetic mutations can distort reaction of an organism on environmental cues and change control parameters of its life cycle. As a result such mutants in laboratory may partly demonstrate life traits similar to those observed in natural environment, e.g. associated with high stress resistance and low rate of aging. These features combined with low external mortality in laboratory conditions may lead to significant extension in the life span of mutants. Recently we considered 56 life-extending gene modifications in nematode C. elegans (Adv. Gerontol., 2003, Vol. 11), scattered in many publications. In this paper we consider pertinent life-extending gene modifications corresponded to the budding yeast S. cerevisease (29 genes), fruit fly D. melanogaster (22 genes) and laboratory mice M. musculus (8 genes).