Last modified: 2014-04-01
Abstract
Evolution is not a continuous process, it is composed of long stabilization periods and intensive changes which result in adaptation to the new niche and speciation. During the stabilization periods, most activity which causes structural changes in the genome negatively affects the survivability of specimens and of the whole population.
However, in presence of environmental stress caused for example by climate change, or by colonization of new environmental niches, introduction of new sources of variability may be beneficial. Mobile genetic elements (transposons) are DNA segments capable of changing their genomic localization. Such activity is potentially dangerous for host organism, therefore during the stability periods, there are several mechanisms controlling the transposition, such as RNA interference, DNA methylation, histone modification.
Here, as in previous paper, we try to show, that the appearance of stress results in suppression or elimination of these mechanisms, what enables the explosion of transposition activity resulting in structural changes in genomes.
Such changes are undirected and increase, in average, the distance from the current phenotypic optimum. However, in the situation of changing environment they could promote the beneficial genetic innovation on the scale of whole population.
Here, we present a stochastic computational model including spatial effects of transposon proliferation in asexual populations. The model is a spatial extension of work previously presented in the paper “Genomic parasites or symbionts? Modeling the effects of environmental pressure on transposon activity in asexual populations” (Theoretical Population Biology). The model uses a Fisher geometric phenotypic landscape with standard Gaussian selection. Mutations are Gaussian as well, but they are affected by transposon activity in order to enable us to study, the interplay between transposition rate and environmental stress. Several scenarios are studied, among them a geographical spread of population to new environments, a colonization of new subniche by an already established species and evolutions of conditions of gradually changing environment.
The strength of this model lies in the fact that, unlike in previous transposition-selection equilibrium-based models, there is no direct relation between the transposon count and the organism’s fitness function (the only link is the transposons’ influence on the mutation rate).
We shall present how the environmental stress and spatial effects stimulate transposon activity.
In particular, we will present how our model predicts several real-world phenomena, such as increased transposon counts in species colonizing new environments as well as increased transposon counts on the frontline of colonization wave.