Hydra vulgaris are some of the simplest animals with neurons and have only two thin, near transparent layers of tissue: myo-endodermal and myo-ectodermal layers. Each cell in the animal can be examined simultaneously due to their small size, simple body pattern, and stereotypical (regular and defined) behaviors. This makes Hydra great animals for examining simple signal transmission pathways from which the complex pathways in vertebrates derive. Cells in the ectoderm and endoderm use calcium signaling to coordinate contractions and cause the animal to move, but how this mechanism of cell-to-cell calcium signaling functions is not well understood. Invertebrate gap junctions, intercellular proteins that cells use to send signals to adjacent cells, are coded from the innexin gene family. It has been found that the genome of Hydra magnipapillata has fourteen predicted innexin genes. Recent data suggests some of these innexins are expressed in the ectoderm, specifically innexins 1,4,5, and 13. I hypothesize these proteins are necessary for the animal to perform coordinated contractions. To determine the role of these proteins, I used shRNA techniques to knockdown innexin expression. After examining wild type Hydra, I examined an existing line of transgenic Hydra which express GCaMP in ectodermal cells to identify when cells use calcium to signal other cells. In these animals, signals can be viewed as a wave of fluorescence passing across the ectoderm. I knocked down the genes by electroporating shRNA molecules into adult animals who express GCaMP, and will image these animals’ behavior. There should be quantifiable differences in the fluorescent waves, as I postulate that some cells will be excluded from these waves if an innexin is knocked down, and analyzing these differences should clarify the role of innexins in gap junction signaling.