Meiosis is a tightly regulated series of events leading to the production of genetically distinct haploid gametes. A key player in this process is the cysteine protease separase (SEP-1). Known for its canonical role in chromosome segregation, recent studies suggest that SEP-1 has an additional function in vesicular trafficking during cell division. We hypothesize that cell cycle machinery known to control SEP-1 protease activity for chromosome segregation also controls its localization to the cortex and subsequent exocytic activity. Following spindle attachment and chromosome alignment during the meiotic M phase, the anaphase promoting complex/cyclosome (APC/C) is activated resulting in the degradation of SEP-1 inhibitory chaperone securin (IFY-1) and entry into anaphase I. In recent studies, we have observed that SEP-1 localizes to specialized vesicles called cortical granules and regulates their exocytosis during anaphase I. Cortical granule exocytosis is necessary for the process of eggshell formation. Before it appears on cortical granules, SEP-1 localizes to cytosolic filaments near the plasma membrane. We have shown that SEP-1 colocalizes with its inhibitor, IFY-1, on filaments during prometaphase, and both disassociate from these structures after the onset of anaphase I. Inhibition of APC/C activity prevents SEP-1 and IFY-1 from leaving the filaments, These data suggest the hypothesis that degradation of IFY-1 may regulate SEP-1 localization to vesicles. IFY-1 depletion does not prevent SEP-1 localization to cortical granules although exocytosis is impaired. To address whether IFY-1 degradation is required to allow SEP-1 translocation onto vesicles, we generated a non-degradeable IFY-1 (IFY-1DM::GFP). Consistent with enhanced IFY-1 stability, IFY-1DM::GFP is not completely degraded following anaphase I onset, remaining on chromosomes and in the cytoplasm into anaphase II. As expected, expression of IFY-1DM::GFP causes embryonic lethality. Additionally, IFY-1DM::GFP localizes to filaments normally and persists longer on these structures and chromosomes than wild type IFY-1 following the resumption of meiosis I. Interestingly, IFY-1DM::GFP causes polar body extrusion failure, which could be related to defects in cortical granule exocytosis. In the future we will investigate how IFY-1DM::GFP affects SEP-1 localization to cortical granules. This will provide insight into how key regulatory components of the cell cycle control SEP-1 localization to promote timely cortical granule exocytosis during anaphase I.