Gene Expression in American Lobster (Homarus americanus) with Epizootic Shell Disease

Abstract

Epizootic 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.

Complex etiologies of emerging diseases in lobsters (Homarus americanus) from Long Island Sound

“…Animals from ELIS have a reduced immune capacity compared with lobsters from Maine or WLIS (Homerding et al 2012), but it is unclear what factors have caused the reduced capacity and whether animals with ESD develop a weakened response prior to the onset of disease. Key synthetic pathways are altered in affected animals, particularly arginine kinase, CYP45, and ecdysteroid receptor synthesis (Tarrant et al 2012). Lobsters with ESD can molt out of the disease, but some animals rapidly recontract the disease after molting (Castro and Angell 2000).…”

Fine-scale transition to lower bacterial diversity and altered community composition precedes shell disease in laboratory-reared juvenile American lobster

“…Lobsters affected by shell disease are energetically compromised, with disruptions to their metabolism and hormone signaling (Tarrant et al 2012). They also tend to have high levels of the molting hormone ecdysone, which can disrupt their reproductive cycle (Laufer et al 2005).…”

Modeling shell disease in American lobster (Homarus americanus) as individual-based health trajectories

“…"Health" here is considered a general construct and can be measured in a number of ways, including the presence of shell disease (Tlusty and Metzler 2012;Tlusty et al 2008) or any one of a myriad of hemolymph or physiological parameters (Basti et al 2010;Chang 2005;Robohm et al 2005). Currently, hemolymph protein (Theriault et al 2008), immune function (Homerding et al 2012), and gene expression (Tarrant et al 2012) are all disrupted in lobsters with shell disease. If one of these physiological metrics is adopted, then the lower boundary would be the defined minimum for the parameter in question.…”