The phylum Cnidaria (jellyfish, hydras and anemones) was one of the earliest diverging animal groups and member species have simple, diffuse nervous systems. A trait unique to Cnidaria is specialized stinging cells (nematocysts) that are considered as part of the nervous system. Nematocysts inject complex venoms which include a diverse set of neurotoxins that bind to and block voltage-gated ion channel genes. Perhaps not coincidentally, cnidarians also possess more voltage-gated ion channel genes than any other animal group. Like other cnidarians, sea anemones use their nematocysts to secure small animal prey, yet a group of potential prey fishes (clownfishes) have evolved symbiotic relationships with anemones and live and breed within anemone tentacles. This symbiotic relationship is not well understood.

I used genomic, transcriptomic, and proteomic approaches in three studies to investigate the evolution of cnidarian toxins and potential mechanisms of anemone-clownfish symbiosis. The first study investigates the potential co-evolution of neurotoxins and ion channels in cnidarians. The second study explores toxin gene and protein diversity in clownfish-hosting and non-hosting sea anemones. The third study examines tissue-specific expression of toxin genes in clownfish-hosting and non-hosting sea anemones. Among the 36 cnidarian species investigated in the first study, neurotoxin and ion channel proteins showed phylogenetic evidence of co-evolution. In the second study, toxin diversity was found to be higher in the anemone that hosted clownfish than the one that did not host clownfish; however, in third study, it was found that the overall expression level of the toxins was found to be lower (both in the tentacles and column) of the clownfish hosting anemone than in anemone that did not host a clownfish.

These results suggest that cnidarian neurotoxins co-evolved with their target ion channels; and that anemone-clownfish symbiosis maybe related to lowered expression levels of certain toxins in the anemone.