Meiosis is the specialized form of cell division in which a single DNA replication event is followed by two successive rounds of chromosome segregation to produce haploid gametes. Errors in meiosis can cause aneuploidy, a major cause of both miscarriage and genetic developmental disorders in humans. The meiotic program must be differentially regulated between males and females to generate sperm and eggs. The highly conserved protein, SAMP-1, is required for regulating chromosome segregation during C. elegans spermatogenesis, but not oogenesis. samp-1(tm2710) mutant hermaphrodites show complete sterility. However, sterility of the samp-1(tm2710) mutants was rescued by providing wild-type sperm, suggesting the sterility phenotype is largely sperm-dependent. SAMP-1 is a 588 amino acid predicted transmembrane protein embedded in the inner nuclear membrane. By immunofluorescence, SAMP-1 is detected at the nuclear periphery in the germ lines of both males and hermaphrodites using an antibody generated against amino acids 338-555. Interestingly, SAMP-1 undergoes a dynamic shift in localization during male meiosis. At the end of prophase I in the male germ line, SAMP-1 begins to localize in the nucleoplasm and by metaphase I becomes concentrated on bivalent chromosomes at the interface between homologs. Preliminary evidence suggests that this change in localization is regulated by proteolytic cleavage. We are using CRISPR gene editing techniques to fluorescently tag SAMP-1 at the N-terminus, C-terminus, and an internal site to determine the mechanisms underlying dynamic localization in the male germ line. Lastly samp-1(tm2710) mutant males exhibit defects in meiotic spindle formation. To monitor these highly dynamic processes, we are using live-cell imaging to capture meiotic cell division in real time to characterize the dynamics of the defects that are observed in samp-1(tm2710) mutant males. samp-1(tm2710) mutant males show a hypomorphic phenotype during anaphase I of meiosis in which severe segregation defects are present in 66% of observed divisions. Defects include shortened metaphase spindles, multiple lagging chromosomes, delayed anaphase, and inappropriate centrosome separation. Interestingly, in the observed “normal” divisions in samp-1(tm2710) mutant males which lack the above defects, anaphase I occurred faster than in wild type. Severe anaphase defects suggest that SAMP-1 is playing a role in regulating cohesion release and/or kinetochore attachments.