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Although accumulation of molecular damage is suggested to be an importantmolecular mechanism of aging, a quantitative link between the dynamics ofdamage accumulation and mortality of species has so far remained elusive. Toaddress this question, we examine stability properties of a generic generegulatory network (GRN) and demonstrate that many characteristics of aging andthe associated population mortality rate emerge as inherent properties of thecritical dynamics of gene regulation and metabolic levels. Based on theanalysis of age-dependent changes in gene-expression and metabolic profiles inDrosophila melanogaster, we explicitly show that the underlying GRNs are nearlycritical and inherently unstable. This instability manifests itself as aging inthe form of distortion of gene expression and metabolic profiles with age, andcauses the characteristic increase in mortality rate with age as described by aform of the Gompertz law. In addition, we explain late-life mortalitydeceleration observed at very late ages for large populations. We show thataging contains a stochastic component, related to accumulation of regulatoryerrors in transcription/translation/metabolic pathways due to imperfection ofsignaling cascades in the network and of responses to environmental factors. Wealso establish that there is a strong deterministic component, suggestinggenetic control. Since mortality in humans, where it is characterized best, isstrongly associated with the incidence of age-related diseases, our findingssupport the idea that aging is the driving force behind the development ofchronic human diseases.

Critical dynamics of gene networks is a mechanism behind ageing and Gompertz law