The role of genome and gene regulatory network canalization in the evolution of multi-trait polymorphisms and sympatric speciation

Kirsten Hwj Ten Tusscher,Paulien Hogeweg

doi:10.1186/1471-2148-9-159

Kirsten Hwj Ten Tusscher, Paulien Hogeweg

Open Access

https://doi.org/10.1186/1471-2148-9-159

Copy DOI

Abstract

BackgroundSexual reproduction has classically been considered as a barrier to the buildup of discrete phenotypic differentiation. This notion has been confirmed by models of sympatric speciation in which a fixed genetic architecture and a linear genotype phenotype mapping were assumed. In this paper we study the influence of a flexible genetic architecture and non-linear genotype phenotype map on differentiation under sexual reproduction.We use an individual based model in which organisms have a genome containing genes and transcription factor binding sites. Mutations involve single genes or binding sites or stretches of genome. The genome codes for a regulatory network that determines the gene expression pattern and hence the phenotype of the organism, resulting in a non-linear genotype phenotype map. The organisms compete in a multi-niche environment, imposing selection for phenotypic differentiation.ResultsWe find as a generic outcome the evolution of discrete clusters of organisms adapted to different niches, despite random mating. Organisms from different clusters are distinct on the genotypic, the network and the phenotypic level. However, the genome and network differences are constrained to a subset of the genome locations, a process we call genotypic canalization. We demonstrate how this canalization leads to an increased robustness to recombination and increasing hybrid fitness. Finally, in case of assortative mating, we explain how this canalization increases the effectiveness of assortativeness.ConclusionWe conclude that in case of a flexible genetic architecture and a non-linear genotype phenotype mapping, sexual reproduction does not constrain phenotypic differentiation, but instead constrains the genotypic differences underlying it. We hypothesize that, as genotypic canalization enables differentiation despite random mating and increases the effectiveness of assortative mating, sympatric speciation is more likely than is commonly suggested.

Highlights

Sexual reproduction has classically been considered as a barrier to the buildup of discrete phenotypic differentiation
Phenotypic diversity under random mating Phenotypic divergence In the full model, but not in the null model, we find the evolution of discrete phenotypic diversity under random mating
For each upstream regulatory region (URR) we show a maximum of 3 transcription factor binding sites (TFBSs), in the rare case that a gene has more TFBSs these are ignored in this Figure

Summary

Introduction

Sexual reproduction has classically been considered as a barrier to the buildup of discrete phenotypic differentiation This notion has been confirmed by models of sympatric speciation in which a fixed genetic architecture and a linear genotype phenotype mapping were assumed. Disruptive selection can be caused by a variety of ecological processes, such as resource competition, frequency dependent predation, sexual conflict and multiple-niche environments [1,2] Adaptive radiations, such as the ones leading to the diverse species flocks of (page number not for citation purposes). The idea is that if any divergence occurs, mating between different parents will lead to hybrid offspring that are an unfit amalgam of the diverged parental properties, destroying the built up divergence This view has been confirmed by various modelling studies. In classical models of obligate sexual organisms it has been demonstrated that evolution of distinct phenotypic divergence requires the evolution of assortative mating leading to sympatric speciation [5,6,7,8,9] (an exception being [1,10])

Methods

Results

Discussion

Conclusion