Date of Completion


Embargo Period



Sodium Channel, Alternative Splicing, Tolerance, Paralytic Shellfish Toxins, Fitness, Selection

Major Advisor

Dr. Hans Dam

Associate Advisor

Dr. David Avery

Associate Advisor

Dr. Carl Schlichting

Associate Advisor

Dr. Senjie Lin

Associate Advisor

Dr. Christopher Gobler

Field of Study



Doctor of Philosophy

Open Access

Open Access


A critical challenge for aquatic scientists is to understand how grazer populations will respond to the proliferation of toxic algal blooms. Previous studies suggest that a novel mutation in the voltage-gated sodium channel of the copepod grazer Acartia hudsonica accounts for its evolutionary adaptation to the toxic dinoflagellate Alexandrium spp. I hypothesized that expression of the mutant sodium channel isoform is adaptive for copepods challenged with toxic Alexandrium spp.

To test this hypothesis I first compared fitness proxies and isoform expression measurements of individual copepods as a function of toxin dose. Since both wild-type and mutant isoforms are always expressed, I partitioned individuals into three expression groups: predominantly mutant (PMI), predominantly wild-type (PWI), or equal proportion (EI) isoforms. There was no consistent evidence that the mutant isoform was advantageous in a toxic environment for ingestion rate, egg production rate, nor gross growth efficiency. In the absence of toxic food, there was no cost associated with the mutant isoform. Lastly, no trade-offs were observed across environments. These results do not support the hypothesis that the mutant isoform is adaptive.

Next, I determined if the mutant isoform was inducible or the target of selection exerted by toxic A. fundyense. Individual expression of mutant isoforms did not differ among groups fed toxic or non-toxic food after six days. During a multi-generation experiment, increases in fitness-related traits for individuals continuously exposed to toxic food were observed; however, selection for PMI individuals did not occur after four generations. These observations are not consistent with the hypothesis that the mutant isoform is associated with adaptation in A. hudsonica populations.

Finally, I corroborated the laboratory experiments with field observations. There were no differences in individual isoforms among populations historically exposed and naïve to toxic Alexandrium spp., or with time within each. No consistent evidence demonstrated that a natural toxic Alexandrium spp. bloom selected for the mutant isoform. These results are consistent with the laboratory findings.

This study repeatedly demonstrated that the mutant sodium channel isoform is not adaptive for Acartia hudsonica under toxic conditions. Other mechanisms of adaptation should be explored.