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تسجيل مستخدم جديدLove kills: Simulations in Penna Ageing Model
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The standard Penna ageing model with sexual reproduction is enlarged by adding additional bit-strings for love: Marriage happens only if the male love strings are sufficiently different from the female ones. We simulate at what level of required difference the population dies out.
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No abstract needed since short
If in the sexual Penna ageing model conditions are applied leading to complementary bit-strings, then marriages between brothers and sisters, or between close cousins, may lead to more offspring than for unrelated couples.
In simulations of sexual reproduction with diploid individuals, we introduce that female haploid gametes recognize one specific allele of the genomes as a marker of the male haploid gametes. They fuse to zygotes preferrably with male gametes having a
different marker than their own. This gamete recognition enhances the advantage of complementary bit-strings in the simulated diploid individuals, at low recombination rates. Thus with rare recombinations the bit-string evolve to be complementary; with recombination rate above about 0.1 instead they evolve under Darwinian purification selection, with few bits mutated.
The population in the sexual Penna ageing model is first separated into several reproductively isolated groups. Then, after equilibration, sexual mixing between the groups is allowed. We study the changes in the population size due to this mixing and
interpret them through a counterplay of purifying selection and of haplotype complementarity.
The expansion of deleted mitochondrial DNA (mtDNA) molecules has been linked to ageing, particularly in skeletal muscle fibres; its mechanism has remained unclear for three decades. Previous accounts assigned a replicative advantage to the deletions,
but there is evidence that cells can, instead, selectively remove defective mtDNA. We present a spatial model that, without a replicative advantage, but instead through a combination of enhanced density for mutants and noise, produces a wave of expanding mutations with wave speed consistent with experimental data, unlike a standard model based on replicative advantage. We provide a formula that predicts that the wave speed drops with copy number, in agreement with experimental data. Crucially, our model yields travelling waves of mutants even if mutants are preferentially eliminated. Justified by this exemplar of how noise, density and spatial structure affect muscle ageing, we introduce the mechanism of stochastic survival of the densest, an alternative to replicative advantage, that may underpin other phenomena, like the evolution of altruism.
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