Woods Hole Oceanographic Institution

Tim Verslycke

»Copepod diapause
»Lobster Shell Disease
»Crustacean molting receptor
»Lobster Shell Disease
»Mysids as test models for endocrine disruption testing
»Chlorotriazines in the Scheldt estuary
»Energy allocation in grasshopper
»Estrogens in Scheldt estuary
»Marsupial development in mysids to evaluate endocrine disruption
»B[a]P effects on steroid metabolism in mysid
»Ciona CYP3 genes
»Methoprene, nonylphenol, and estrone effects on mysid vitellogenesis
»Methoprene effects on mysid molting
»Mysid growth
»Mysid vitellin ELISA
»Mysid vitellin
»An analytical method to detect estrogens in water
»High levels of endocrine disruptors in wild mysid populations
»Energy allocation in wild mysid populations
»Cellular energy allocation validation with scope for growth
»Dolphin delivery prediction
»PhD thesis
»Endocrine disruptor effects on steroid and energy metabolism in mysid
»Mysid review
»TBT effects on steroid metabolism in mysid
»Metal mixture toxicity to mysid
»TBT effects on energy metabolism in mysid
»dichlorobenzene effects in zebrafish
»Ethinylestradiol effects on amphipod sexual development
»Metabolic studies with mysids
»Abiotic stress and energy metabolism in mysid
»Induced vitellogenesis in rainbow trout
»Steroid metabolism in mysid
»Endocrine disruption in freshwater snails
»Invasive mysid in Belgium

Ann M. Tarrant, Diane G. Franks, and Tim Verslycke, Gene expression in American lobster (Homarus americanus) with epizootic shell disease, Journal of Shellfish Research - special issue, submitted

Epizootic shell disease (ESD) has been reported widely in American lobster (Homarus americanus) inSouthern New England. The appearance of irregular deep lesions, characteristic of ESD, has previously been associated with elevated levels of ecdysteroids and premature molting, but the underlying molecular and physiological changes associated with ESD remain poorly understood. Previously, we identified several genes, including arginine kinase and hemocyanin, that were differentially expressed in symptomatic ('diseased') versus asymptomatic (assumed 'healthy') lobsters and quantified their expression. In this study, we extend these findings and measured expression of a suite of 12 genes in tissues from 36 female lobsters of varying disease condition. In addition, molt stage was evaluated as a possible confounding factor in the expression of the selected genes. The expression of several genes changed significantly with disease stage. Arginine kinase expression significantly decreased in thoracic muscle of symptomatic lobsters. Ecdysteroid receptor expression was significantly elevated in both muscle and hepatopancreas of symptomatic lobsters. CYP45, a cytochrome P450 form that was previously shown to co-vary with ecdysteroid levels and to be inducible by some xenobiotics, showed significantly increased expression in hepatopancreas of symptomatic lobsters. Together these results demonstrate that the expression of several genes is altered in lobsters showing symptoms of ESD, even when accounting for variation in molt stage. Given the observed changes in ecdysteroid receptor, arginine kinase, and CYP45 expression, further investigations of the association, if any, between molting, muscular function and xenobiotic metabolism and ESD are warranted.

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