A Gene Regulatory Model of heterosis and speciation

A Gene Regulatory Model of heterosis and speciation
Peter M. F. Emmrich, Vera Pancaldi, Hannah E. Roberts, Krystyna A. Kelly, David C. Baulcombe
(Submitted on 15 Sep 2013)

Crossing individuals from genetically distinct populations often results in improvements in quantitative traits, such as growth rate, biomass production and stress resistance; this phenomenon is known as heterosis. We have taken a computational approach to explore the mechanisms underlying heterosis, developing a simulation of evolution and hybridization of Gene Regulatory Networks (GRNs) in a Boolean framework. These artificial regulatory networks exhibit biologically realistic topological properties and fitness is measured as the ability of a network to respond to external inputs in the correct way. Our model reproduced experimental observations from the literature on heterosis using only biologically meaningful parameters, such as mutation rates. Hybrid vigor was observed, its extent was seen to increase as parental populations diverged until it collapses when the two populations have become incompatible. Thus, the model also describes a process of speciation and links it to collapsing hybrid fitness due to genetic incompatibility of the separated populations. We also reproduce for the first time in a model the fact that hybrid vigor cannot easily be fixed by crossing hybrids, which is currently an important drawback of the use of hybrid crops. The simulation allows us to study the effects of three standard models for the genetic basis of heterosis, dominance, over-dominance, and epistasis. In our simulation over-dominance is the main factor contributing to hybrid vigour, whereas under-dominance and epistatic incompatibility are responsible for the fitness collapse. As the parental populations diverge, a single mutation can determine an almost sudden incompatibility leading to low fitness hybrids.

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