help button home button Genetics J Clin Inv
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

Originally published as Genetics Published Articles Ahead of Print on October 18, 2007.

Genetics, Vol. 177, 1777-1790, November 2007, Copyright © 2007
doi:10.1534/genetics.107.074393

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Data Supplement
Right arrow All Versions of this Article:
genetics.107.074393v1
177/3/1777    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Tellier, A.
Right arrow Articles by Brown, J. K. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Tellier, A.
Right arrow Articles by Brown, J. K. M.

Polymorphism in Multilocus Host–Parasite Coevolutionary Interactions

Aurélien Tellier1 and James K. M. Brown

Department of Disease and Stress Biology, John Innes Centre, Colney, Norwich, NR4 7UH, United Kingdom

1 Corresponding author: Section of Evolutionary Biology, Biocenter, University of Munich, 82152 Planegg-Martinsried, Germany.
E-mail: tellier{at}zi.biologie.uni-muenchen.de

Numerous loci in host organisms are involved in parasite recognition, such as major histocompatibility complex (MHC) genes in vertebrates or genes involved in gene-for-gene (GFG) relationships in plants. Diversity is commonly observed at such loci and at corresponding loci encoding antigenic molecules in parasites. Multilocus theoretical models of host–parasite coevolution predict that polymorphism is more likely than in single-locus interactions because recurrent coevolutionary cycles are sustained by indirect frequency-dependent selection as rare genotypes have a selective advantage. These cycles are stabilized by direct frequency-dependent selection, resulting from repeated reinfection of the same host by a parasite, a feature of most diseases. Here, it is shown that for realistically small costs of resistance and virulence, polycyclic disease and high autoinfection rates, stable polymorphism of all possible genotypes is obtained in parasite populations. Two types of epistatic interactions between loci tend to increase the parameter space in which stable polymorphism can occur with all possible host and parasite genotypes. In the parasite, the marginal cost of each additional virulence allele should increase, while in the host, the marginal cost of each additional resistance allele should decrease. It is therefore predicted that GFG polymorphism will be stable (and hence detectable) when there is partial complementation of avirulence genes in the parasite and of resistance genes in the host.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2007 by the Genetics Society of America.