Both snail and parasite genes determine the susceptibility of the snail Biomphalaria glabrata to infection with the trematode Schistosoma mansoni. To identify molecular markers associated with resistance to the parasite in the snail host, we performed genetic crosses between parasite-resistant and -susceptible isogenic snails. Because resistance to infection in adult snails is controlled by a single locus, DNA samples from individual F 2 and F 1 backcross progeny, segregating for either the resistant or susceptible phenotypes, were pooled (bulked segregant). Genotypes for both parents were determined with 205 arbitrary decamer primers by random amplified polymorphic DNA-PCR. Of the 205 primers, 144 were informative, and the relative allele frequencies between the pools for these primers were determined. Two primers, OPM-04 and OPZ-11, produced fragments in the resistant parent of one cross that were inherited in a dominant fashion in the resistant F 2 and backcross-bulked segregant progeny. Subsequent typing of DNA samples of individual progeny snails showed that the 1.2-kb marker amplified by primer OPM-04 and the 1.0-kb marker produced by primer OPZ-11 segregated in the same dominant fashion with the resistant phenotype. Sequence analysis of the 1.2-kb marker showed that it corresponds to a repetitive sequence in the snail genome with no homology to existing DNA sequences in the public databases. Analysis of the 1.0-kb marker showed that it also corresponds to a repetitive sequence in the B. glabrata genome that contains an imperfect ORF, with homology to retrovirus-related group-specific antigens (gag) polyprotein.

In an effort to investigate the 'flow' of parasite-resistance genes through laboratory snail populations, we determined the susceptibility of progeny snails from freely interbreeding parasite-susceptible and parasite-resistant parents. Five parental populations of Biomphalaria glabrata were used to generate the progeny snails. Three of them contained different proportions of Schistosoma mansoni-susceptible albino snails (NMRI stock) and S. mansoni-resistant pigmented snails (BS-90), while single stock controls comprised the other two parental populations. F(1) snails from each parental population were exposed to S. mansoni miracidia. Some of the progeny snails were exposed as juveniles, others as adults. According to Hardy-Weinberg principle predictions, the F(1) generation from the three pigmented/albino parental populations displayed higher than expected numbers of pigmented (resistant) snails and lower than expected numbers of albino (susceptible) snails. Among the assumptions of the Hardy-Weinberg principle that were not met within these populations could include non-random mating, unequal fecundity, different hatching and survival rates of different genotypes, or other life-history differences between snail stocks. It is clear, though, that for these two laboratory snail stocks there is no fitness cost attached to genetic resistance to the parasite.

Biomphalaria glabrata is a major intermediate host for the helminth parasite Schistosoma mansoni. Beginning in the mid-20th century, studies were carried out with this snail species to identify the immunological and genetic components that might be involved in controlling schistosome development. A number of genetically well-defined snail stocks were derived as a direct result of these studies and have since played major roles in helping investigators to identify important cellular and humoral components in the snail/schistosome relationship. This review will explore the historical development of these stocks and describe some of the major advances in several areas of medical malacology that hawe been made possible be their use.