Joost B Beltman | Search PubMed

PubMed2004

MHC polymorphism under host-pathogen coevolution.

The genes encoding major histocompatibility (MHC) molecules are among the most polymorphic genes known for vertebrates. Since MHC molecules play an important role in the induction of immune responses, the evolution of MHC polymorphism is often explained in terms of increased protection of hosts against pathogens. Two selective pressures that are thought to be involved are (1) selection favoring MHC heterozygous hosts, and (2) selection for rare MHC alleles by host-pathogen coevolution. We have developed a computer simulation of coevolving hosts and pathogens to study the relative impact of these two mechanisms on the evolution of MHC polymorphism. We found that heterozygote advantage per se is insufficient to explain the high degree of polymorphism at the MHC, even in very large host populations. Host-pathogen coevolution, on the other hand, can easily account for realistic polymorphisms of more than 50 alleles per MHC locus. Since evolving pathogens mainly evade presentation by the most common MHC alleles in the host population, they provide a selective pressure for a large variety of rare MHC alleles. Provided that the host population is sufficiently large, a large set of MHC alleles can persist over many host generations under host-pathogen coevolution, despite the fact that allele frequencies continuously change.

Computer Simulation↗

PubMed2004

Learning and colonization of new niches: a first step toward speciation.

Learning processes potentially play a role in speciation but are often ignored in speciation models. Learning may, for instance, play a role when a new niche is being colonized, because the learning of niche features may cause niche-specific assortative mating and a tendency to produce young in this niche. Several animal species learn about their environmental features that may be important in finding or attracting mates. We use a gene-culture coevolutionary model to look into the effect of such learning on the colonization of new niches and on the genetic divergence between groups using different niches, which are steps necessary in achieving speciation. We assume that density is regulated separately in each of the two niches and that the viability of an individual depends on its genotype as well as on which niche it exploits. Our results show that genetic adaptation to the new niche is enhanced by a high female fecundity and a low viability selection against heterozygotes. Furthermore, when initial colonization (without genetic adaptation) fails, genetic divergence is more difficult when the mating preference is stronger. In contrast, when colonization without genetic adaptation is successful, a stronger mating preference makes genetic divergence easier. An increase in the number of egg-laying mistakes by females can have a positive or negative effect on the success of genetic adaptation depending on other parameters. We show that genetic divergence can be prevented by a niche shift, which can occur only if viabilities in the two niches are asymmetrical.

Adaptation, Biological↗