The role of genome and gene regulatory network architecture in the evolution of multi-trait polymorphism and sympatric speciation. Canalization increases the robustness to recombination
Friday seminar by Kirsten ten Tusscher.
In simple "gene bag" models in which genes code in a simple additive manner for the properties of organisms and genes assort randomly to the next generation, the occurrence of sexual reproduction severely limits the buildup of genotypic and phenotypic diversity in the population. Under random mating a single peaked phenotype distribution will arise and on the long term polymorphisms will be restricted to a limited number of loci. The formation of multiple distinct phenotype peaks requires assortative mating which will lead to sympatric speciation.
Clearly, these model predictions do not agree well with what we see in nature, as many species contain stable multi-trait polymorphisms and the distinction between polymorphism and specation is a gradual rather than a discrete one. To overcome these problems, more complex epistatic interactions and linkage between genes should be taken into account. We do this rather explicitly by using an individual based model in which organisms contain a genome with genes and transcription factor binding sites. This genome codes for a gene regulatory network that determines the expression states of the genes. These expression states are taken as the phenotype of the organisms.
Using our model we show that under random mating, a stable multi trait polymorphism readily evolves. In addition we show that if assortative mating is allowed to evolve, not only do high levels of assortativeness evolve but assortativeness also becomes highly effective. We demonstrate that the genome to network to phenotype mapping in our model, and the fact that both the organization of the genome and the network can evolve allows for a genetic canalization process that restricts differences between the genomes and networks of different morphs/species to a limited number of locations. This canalization leads to an increased robustness against recombination, which enables phenotypic divergence despite sexual reproduction.
Kirsten ten Tusscher