Brugia malayi, a parasitic filarial nematode that causes lymphatic filariasis in humans,maintains an obligate symbiotic relationship with the gram-negative α-proteobacterium Wolbachia pipientis. Elimination of W. pipientis from B. malayi induces fertility defects and kills the matured worms. Therefore, understanding the molecular mechanisms by which W. pipientis colonizes the tissues of B. malayi will inform drug discovery efforts against lymphatic filariasis. Because of the intractable nature of the organisms’ symbiotic relationship, it has been difficult to study the specific molecular mechanisms by which Wolbachia colonizes B. malayi. However, Wolbachia is proposed to secrete effector proteins via a functional type IV secretion system to survive in the cells of B. malayi. During periods of rapid B. malayi growth in humans, W. pipientis increase in number in the nematode’s hypodermal and reproductive tissues, where there is an upsurge in the expression levels of Wolbachia secreted proteins. Screening of these secreted protein in Saccharomyces cerevisiae identified several that cause defects in S. cerevisiae growth and physiology. Particularly, expression of recombinant wBm0076 in S. cerevisiae causes a severe growth defect. Curiously, bioinformatic analyses suggest Wbm0076 is an effector that belongs to the eukaryotic Wiskott-Aldrich syndrome (WASp) family of proteins involved in remodeling the actin cytoskeleton of eukaryotic cells. Therefore, Wbm0076 may play an active role in Wolbachia invasion of host cells via actin pathways. We focus here on characterizing Wbm0076 via molecular and biochemical assays in the surrogate eukaryotic cell model S. cerevisiae to further our understanding of the function of the secreted effector.