We have demonstrated that the expression of the ELP in our strains is the outcome of a genetically determined, environmentally modulated, event dependent, developmental process. Given the appropriate genetic and environmental conditions, we observe an early acting temporal progression of alterations in specific gene activity patterns which appear to give rise to functional phenotypic changes. The observed patterns are consistent with the interpretations drawn from our chromosome substitution and biomarker experiments. The interaction of specific environmental and genetic factors is sufficient to explain the observed plasticity of longevity in our L strain. Independently derived long lived strains may have altered different combinations of physiological mechanisms so as to give rise to a statistically equivalent ELP. Theoretically based conclusions obtained from only one set of sister strains may be difficult to extrapolate to other strains. Future work will involve the experimental verification of the genetic-environmental circuitry discussed here, using novel molecular genetic techniques to define, characterize, and isolate the genes involved in the expression of the ELP.