Genetic and phenotypic variation associated with the resistance gene SOD1 in Biomphalaria glabrata, an important intermediate host of Schistosomiasis Public Deposited

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  • Schistosomiasis afflicts 200 million people and is responsible for 200,000 deaths per year. The infection is caused by a digenean trematode in the genus Schistosoma. The parasite must cycle through both a vertebrate (human) and invertebrate (snail) host to complete the life cycle. My dissertation focuses on the genetic mechanisms of resistance in the snail intermediate host Biomphalaria glabrata to the parasite Schistosoma mansoni. Understanding the underlying mechanisms controlling resistance in the intermediate host is essential for elucidating transmission dynamics and the development of appropriate biological control techniques. Much of what we know about the resistance of the intermediate host has been determined using established laboratory strains of both the snail and trematode species. The B. glabrata/S. mansoni system serves as a model system for studying schistosomiasis. Resistance to parasite infection in the snail is highly heritable. While many genes have been implicated, allelic variation correlating with resistance has only been observed at a single gene, copper-zinc superoxide dismutase (SOD1). SOD1 is functionally relevant because it catalyzes the conversion of the highly reactive superoxide into the less reactive hydrogen peroxide and water. In the snail, hydrogen peroxide is released as part of the immune response to the invading parasite. The goal of my dissertation was to further evaluate SOD1 as a resistance locus. In the second chapter I examined allelic variation at SOD1 and looked for evidence of selection on SOD1 in natural populations of B. glabrata. To determine the utility of SOD1 as a resistance locus in natural populations, we needed to first determine if there was indeed allelic variation in natural population of B. glabrata. This is important because if the alleles do not co-occur in natural populations, then the relative selective advantage of one allele over another in terms of resistance would be of little ecological relevance in natural transmission zones. Variation at SOD1 in natural populations cannot be assumed because the initial study describing the correlation between resistance to infection and allelic variation used a hybrid laboratory strain of B. glabrata (13-16-R1). Therefore, we did not know if the co-occurrence of particular alleles at SOD1 in the 13-16-R1 lab strain was a natural phenomenon or is an artifact of the breeding history of the strain. In this study we were able to identify the likely geographic origins of the alleles in the lab strain 13-16-R1 and determine that different alleles do co-occur in some natural populations. Additionally, we found heterozygote excess at SOD1 in all the populations segregating for the allele that confers highest resistance in 13-16-R1. This result raises the possibility that overdominance is acting at SOD1 or some locus closely linked to it.
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