TitleThree genes involved in the oxidative burst are closely linked in the genome of the snail, Biomphalaria glabrata
Publication TypeJournal Article
Year of Publication2013
AuthorsBlouin, M, Bonner, KM, Cooper, B, Amarasinghe, V, O'Donnell, RP, Bayne, CJ
JournalInternational Journal for Parasitology
Volume43
Pagination51-55
Type of ArticleJournal Article
ISSN0020-7519
Abstract

Allelic variation at the Cu-Zn superoxide dismutase (SOD)) locus has been shown to be associated with resistance of the snail, Biomphalaria glabrata, to infection by the trematode parasite, Schistosoma mansoni. SOD) catalyses the production of hydrogen peroxide, a known cytotoxic component of the oxidative burst used in defence against pathogens. In our laboratory population of B. glabrata, the most resistant allele at SOD) is over-expressed relative to the other two alleles. Because hydrogen peroxide also causes oxidative stress on host tissues, we hypothesised that over-expression of SOD1 might be compensated by epistatic interactions with other loci involved in oxidation-reduction (redox) pathways. Catalase, peroxiredoxins and glutathione peroxidases all degrade hydrogen peroxide. We tested whether alleles at each of these loci were in linkage disequilibrium with SOD) in our population, as might be expected given strong epistatic selection. We found that SOD 1, catalase (CAT) and a peroxiredoxin locus (PRX4) are in strong linkage disequilibrium in our population. We also found that these loci are tightly linked, within 1-2 cM of each other, which explains the high linkage disequilibrium. This result raises the possibility that there is a linked cluster of redox genes, and perhaps other defence-relevant genes, in the B. glabrata genome. Whether epistatic interactions for fitness actually exist among these loci still needs to be tested. However the close physical linkage among SOD1. PRX4 and CAT, and subsequent high disequilibrium, makes such interactions a plausible hypothesis. (C) 2012 Australian Society for Parasitology Inc. Published by Elsevier Ltd. All rights reserved.

URL<Go to ISI>://WOS:000314614800006
DOI10.1016/j.ijpara.2012.10.020