In the race to fertilize oocytes, sperm cells encounter extracellular environments that affect their success. These environments include male and female reproductive tracts as well as seminal fluid. In many species, proteolysis regulators are abundant in seminal fluid and contribute to various aspects of fertility. In C. elegans, protease signals regulate the onset of sperm motility, a process called activation that occurs after mating. Spatial and temporal regulation of motility is critical, as either premature or delayed activation results in significantly reduced fertility. During activation, sperm undergo morphogenesis and develop a pseudopod, which they use to crawl toward oocytes. The secreted protease TRY-5 is present in the male gonad and in seminal fluid, where it is required to activate sperm. Upstream of TRY-5, the secreted protease inhibitor SWM-1 is required to inhibit activation, yet how the protease signal is regulated spatially and temporally to control activation is unknown. To understand how SWM-1 regulates activation, we used CRISPR to tag SWM-1 at its endogenous locus. We find that swm-1 is expressed in both the gonad and extra-gonadal cells and that SWM-1 protein surrounds spermatids. In vas deferens cells, SWM-1 localizes to vesicles closely associated with the apical membrane. Surprisingly, it is transferred with TRY-5 during mating. How seminal fluid is secreted from these vesicles is unknown and we are using our SWM-1 reporter to analyze vesicle dynamics. Tissue-specific expression shows that vas deferens-derived SWM-1 is at least partially sufficient to regulate activation. Our findings lead to a model where SWM-1 is secreted from the vas deferens to inhibit TRY-5 from activating sperm until mating. Intriguingly, the presence of SWM-1 in seminal fluid suggests an additional post-mating role in the hermaphrodite. In support of this hypothesis, SWM-1 has two trypsin-inhibitor-like (TIL) domains, which have distinct reactive sites and appear to play non-equivalent roles in inhibiting activation. To further investigate the role of SWM-1 in fertility, we are using CRISPR to generate reactive site mutants and we are testing SWM-1 for post-mating roles within the hermaphrodite reproductive tract.