a1 UMR 5244 CNRS-EPHE-UPVD, Biologie et Ecologie Tropicale et Méditerranéenne, Université Via Domitia. 52 Av. Paul Alduy, 66860 Perpignan Cedex, France
a2 U547 Inserm, Institut Pasteur de Lille, 1 Rue du Prof. Calmette, BP 245, 59019 Lille Cedex, France
a3 EA 3680, Mathématiques et Physique pour les Systèmes (MEPS), Université de Perpignan Via Domitia, 52 Av. Paul Alduy. 66860 Perpignan Cedex, France
a4 Department of Zoology, Oregon State University, Corvallis, OR, 97331 USA
The genetic control of compatibility between laboratory strains of schistosomes and their snail hosts has been studied intensively since the 1970s. These studies show (1) a bewildering array of genotype-by-genotype interactions – compatibility between one pair of strains rarely predicts compatibility with other strains, and (2) evidence for a variety of (sometimes conflicting) genetic mechanisms. Why do we observe such variable and conflicting results? One possibility is that it is partly an artifact of the use of laboratory strains that have been in culture for many years and are often inbred. Here we show that results of compatibility trials between snails and schistosomes – all derived from the same natural population – depend very much on whether one uses laboratory-cultured or field-collected individuals. Explanations include environmental effects of the lab on either host or parasite, and genetic changes in either host or parasite during laboratory culture. One intriguing possibility is that genetic bottlenecks during laboratory culture cause the random fixation of alleles at highly polymorphic loci that control the matched/mismatched status of hosts and parasites. We show that a simple model of phenotype matching could produce dose response curves that look very similar to empirical observations. Such a model would explain much of the genotype-by-genotype interaction in compatibility observed among strains.
(Received April 10 2008)
(Revised May 14 2008)
(Accepted May 14 2008)