Epigenetic contribution to age distribution of mortality within the Penna model

Abstract

Some modifications of the simple asexual Penna model, enriched by epigenetic contributions, are presented. The standard bit-string Penna model of biological aging and population evolution is based on an inherited DNA structure which defines the future life of a newly born individuals, when genes are activated by the biological clock, and the predefined genetic death is fully controlled by the number of defected genes. Epigenomes allow to introduce additional mechanism of gene activation or silencing without affecting the DNA genome itself. It may be either inherited or may reflect external, environmental factors. In the presented model, information read from the introduced epigenome may alter gene expression that may be stopped or re-activated. We concentrate on the influence of epigenetics on the age $a$ distribution of genetic mortality $m(a)$. Changes in $m(a)$ are strong for the case of inherited epigenetic contribution with nearly perfect inheritance and ‘positive’ epigenome that partly ignores the ‘bad’ mutations. We conclude that the epigenetic contribution may influence population structure $m(a)$ and could be, at least partly, responsible for deviation of $m(a)$ distribution from the Gompertz law. In short, we claim that proposed epigenetic contribution may be seen as a candidate for possible explanation of observed deviation from the Gompertz law, also among senior members of society. A very simple model was used in this paper and many crucial mechanisms of biological aging were omitted. Therefore, further work based on a more realistic models is necessary.