Dictyostelium discoideum is a well-established mitochondrial model system for both disease and dynamics, yet we still do not understand the actual mechanism of mitochondrial dynamics in this system. The FtsZ proteins are known to mediate membrane remodeling events such as cytokinesis in bacteria and fission of chloroplasts; D. discoideum has two FtsZ proteins, FszA and FszB. To determine the role of these proteins in mitochondrial dynamics we overexpressed FszB-GFP and determined its effect on fission, fusion, and motility in the presence of intact and disrupted cytoskeletal filaments. Here we show that overexpression of FszB-GFP decreases mitochondrial dynamics and suggest that actin may play a positive role driving fission in the context of excessive inhibition by overexpressed FszB-GFP.