Sodium channel expression in the copepod Acartia hudsonica as a function of exposure to paralytic shellfish toxin (PST)

Local adaptation of the copepod Acartia hudsonica to toxic Alexandrium spp. is associated with degree of historical co-exposure. Recently, a novel mutation in the sodium channel in A. hudsonica was hypothesized to be the mechanism of adaptation to toxic Alexandrium; all copepods express both types of sodium channels. We tested the hypothesis that mutant sodium channel expression in A. hudsonica individuals corresponded to historical co-exposure to A. fundyense. Female A. hudsonica were sampled from historically exposed (Maine) and naïve (Connecticut and New Jersey) populations to A. fundyense, throughout the 2011 season of growth of A. hudsonica. There were no consistent differences in wild-type: mutant isoform ratios nor in the relative abundance of individuals that predominately express one type of isoform, either through time within a population or among populations or over time within each location. We also tested the hypothesis that expression of the mutant sodium channel isoform in A. hudsonica should increase during the progression of a toxic Alexandrium bloom. Sodium channel expression was compared before, during, and after the 2011 toxic Alexandrium spp. bloom in Northport Harbor, NY. Moreover, the relative expression of the mutant isoform increased slightly after the peak of the toxic Alexandrium spp. bloom; however, there was no simultaneous increase in individuals that predominately express mutant channel isoforms. Overall, there was little evidence in support of our hypotheses. Other mechanisms must be responsible for the observed geographic differences in adaptation of copepods to toxic Alexandrium.