The evolution of group-level pathogenic traits.
A group-selection model for the evolutionary origin of phase-variation in E. coli is proposed. Populations of commensal strains of E. coli populating mammalian hosts modulate its immune defenses through population-level control of the expression of fimbriae. At any time only a proportion of the population expresses these cell-surface adhesins. Collectively they elicit a host-based nutrient release if the fimbriae expression is low. Too high levels of fimbriation would provoke an inflammatory response and thus intolerable conditions for the cells. The optimal level of fimbriation is a group property and its evolution is difficult to explain by naive individual selection scenarios. This article presents a computational model to simulate the evolution of fimbriae. The two main conclusions of this contribution are: (i) the evolution of this group property requires the population to be partitioned into weakly interacting sub-populations. (ii) Given certain scenarios evolution consistently under-performs, in the sense that it does not find the optimal level of fimbriation.
Chu
Dominique
D
Computing Laboratory, University of Kent, Cornwallis, Canterbury CT27NF, UK. D.F.Chu@kent.ac.uk <D.F.Chu@kent.ac.uk>
D000222:Adaptation, Physiological; D000818:Animals; D005075:Biological Evolution; D004926:Escherichia coli / Q000235:genetics / Q000472:pathogenicity* / Q000502:physiology; D010861:Fimbriae, Bacterial / Q000235:genetics / Q000502:physiology; D019655:Quantitative Trait, Heritable; D037521:Virulence Factors / Q000235:genetics / Q000502:physiology
D037521:Virulence Factors