Myxozoans are an enigmatic group of obligately parasitic, microscopic cnidarians. They diverged from their free-living relatives over 600 million years ago and have highly reduced genomes. However, they have retained nematocyst stinging cells which characterize the phylum Cnidaria. Free-living cnidarians utilize this cellular weaponry for defense and predation whereas the myxozoans use it to anchor to their hosts as the first step to infection. In this thesis, I explore similarities and differences in the structure and function of nematocysts from myxozoans and free-living cnidarians via a “double-bladed” approach consisting of wet-lab techniques and bioinformatic analyses. In chapter 2, I report my results from two wet-lab assays that I developed to test the effect of chemical treatments on nematocyst discharge and infection, using the model myxozoan Myxobolus cerebralis. I found that Na+ significantly increased discharge and reduced infection to rainbow trout. This finding aligned with prior work using free-living Cnidaria, suggesting divalent cations bound to poly-gamma glutamate inside the nematocyst can be exchanged with monovalent ions from the environment through the capsule wall to promote discharge. In Appendix A, I report my initial results from bioinformatic analyses of proteomic and transcriptomic datasets from the myxozoan Ceratonova shasta, in searches for genes for voltage-gated ion channels. In free-living Cnidarians, these channels play a role in signaling nematocyst discharge and exocytosis of Ca2+. I found that in C. shasta, genes for these channels were co-expressed with nematocyst-specific genes during sporogenesis in the fish host. Taken together, the results of my wet-lab and computational “double-bladed” approach demonstrate structural and functional homologies between the nematocysts of myxozoans and their free-living cnidarian relatives.