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dc.contributor.authorTarrant, Ann M.
dc.contributor.authorFranks, Diana G.
dc.contributor.authorVerslycke, Tim A.
dc.date.accessioned2012-08-16T18:49:44Z
dc.date.available2012-08-16T18:49:44Z
dc.date.issued2012-06
dc.identifier.citationJournal of Shellfish Research 31 (2012): 505-513en_US
dc.identifier.urihttp://hdl.handle.net/1912/5335
dc.descriptionAuthor Posting. © National Shellfisheries Association, 2012. This article is posted here by permission of National Shellfisheries Association for personal use, not for redistribution. The definitive version was published in Journal of Shellfish Research 31 (2012): 505-513, doi:10.2983/035.031.0210.en_US
dc.description.abstractEpizootic shell disease (ESD) has been reported widely in American lobster (Homarus americanus, Milne Edwards) in southern New England. The appearance of irregular, deep lesions—characteristic of ESD—has been associated previously 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 expressed differentially in lobsters exhibiting signs of ESD (diseased) versus those lobsters exhibiting no signs of ESD (assumed healthy), and quantified their expression. In this study, we extend these findings and measure expression of a suite of 12 genes in tissues from 36 female lobsters of varying disease condition. In addition, molt stage is 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 decreased significantly in thoracic muscle of lobsters with signs of ESD. Ecdysteroid receptor expression was elevated significantly in both muscle and hepatopancreas of lobsters with signs of ESD. CYP45, a cytochrome P450 form that was shown previously to covary with ecdysteroid levels and to be inducible by some xenobiotics, showed significantly increased expression in hepatopancreas of lobsters with signs of ESD. Together, these results demonstrate that the expression of several genes is altered in lobsters showing signs 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.en_US
dc.description.sponsorshipThis work was supported by the National Marine Fisheries Service as the New England Lobster Research Initiative: Lobster Shell Disease under NOAA grant NA06NMF4720100 to the University of Rhode Island Fisheries Center.en_US
dc.format.mimetypeapplication/pdf
dc.language.isoen_USen_US
dc.publisherNational Shellfisheries Associationen_US
dc.relation.urihttp://dx.doi.org/10.2983/035.031.0210
dc.subjectArginine kinaseen_US
dc.subject100 lobstersen_US
dc.subjectCytochrome P450en_US
dc.subjectEcdysteroiden_US
dc.subjectEndocrineen_US
dc.subjectHepatopancreasen_US
dc.subjectHeat shock proteinen_US
dc.subjectEpizootic shell diseaseen_US
dc.subjectAmerican lobsteren_US
dc.subjectShadeen_US
dc.titleGene expression in American lobster (Homarus americanus) with epizootic shell diseaseen_US
dc.typeArticleen_US
dc.identifier.doi10.2983/035.031.0210


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