Penna Model Of Aging Research Articles

Cellular senescence in the Penna model of aging

Cellular senescence is thought to play a major role in age-related diseases, which cause nearly 67% of all human deaths worldwide. Recent research in mice showed that exercising mice had higher levels of telomerase, an enzyme that helps maintain telomere length, than nonexercising mice. A commonly used model for biological aging was proposed by Penna. I propose a modification of the Penna model that incorporates cellular senescence and find an analytical steady-state solution following Coe, Mao, and Cates [Phys. Rev. Lett. 89, 288103 (2002)]. I find that models corresponding to delayed cellular senescence have younger populations that live longer. I fit the model to the United Kingdom's death distribution, which the original Penna model cannot do.

SPECIATION EFFECT IN THE PENNA AGING MODEL

We have simulated the evolution of diploid, sexually reproducing populations using the Penna model of aging. We have noted that diminishing the recombination frequency during the gamete production generates a specific diversity of genomes in the populations. When two populations independently evolving for some time were mixed in one environmental niche of the limited size and crossbreeding between them was allowed, the average lifespan of hybrids was significantly shorter than the lifespan of the individuals of parental lines. Another effect of higher hybrid mortality is the faster elimination of one parental line from the shared environment. The two populations living in one environment co-exist much longer if they are genetically separated — they compete as two species instead of crossbreeding. This effect can be considered as the first step to speciation — any barrier eliminating crossbreeding between these populations, leading to speciation, would favor the populations.

HIGHER MORTALITY OF THE YOUNGEST ORGANISMS PREDICTED BY THE PENNA AGING MODEL

We have simulated the evolution of population using the Penna model of aging. In populations of diploid organisms, without recombination between haplotypes or with low cross-over rate, a specific distribution of defective genes has been established. As an effect, relatively higher mortality is observed during the earliest stages of life. When two independently evolving populations were mixed and co-evolved in one environment without crossbreeding, one population won after several generations and this winning population showed stronger "early" death effect. We conclude that in the environmentally limited size of a population (in the model limit set by Verhulst factor) it is a better strategy to sacrifice younger individuals — higher fractions of such populations reach the reproduction age.

HOUSEKEEPING GENES AND DEATH GENES IN THE PENNA AGING MODEL

The Penna model of aging predicts the accumulation of defective genes expressed after the organism reaches the minimum reproduction age in the genetic pool of the population. The accumulation of defects in the genomes implicates the specific age structure of the modeled populations. Nevertheless, the fraction of defective alleles at loci switched on before the reproduction period does not depend on exact age when precisely they are switched on, it may be just after conception or after birth. We have modeled the mortality of a population in the period before the minimum reproduction age, even before birth, assuming that sets of genes of different size are switched on in different periods of the life span.

AGE-OF-PARENT DEPENDENT MUTATION RATE AND WEAK CHILDREN IN THE PENNA MODEL IN BIOLOGICAL AGEING

We investigate the effect of an age-dependent mutation rate in the Penna model of ageing and then we observe that the high mortality for human babies can be reproduced by the model if one assumes babies to be weaker than adults.