Co-ordination of the dynamic chromosomal events during meiosis is critical to ensure accurate chromosome segregation for the next generation. Missegregation of chromosomes during meiosis can cause chromosomal aneuploidies, which result in miscarriage and genetic disorders such as Down syndrome. Previous studies conducted in budding yeast have implied that aurora kinases (AURKs) impact a number of critical events during the meiotic prophase I to metaphase I transition (G2/MI), including the disassembly of the synaptonemal complex (SC) and the faithful production of a bipolar spindle. While the events of meiosis are evolutionarily conserved, the mechanisms for controlling these events can differ markedly between distant species, complicating attempts to bridge findings in lower eukaryotes to humans. For instance, budding yeast expresses a single AURK protein, whereas mammals express three AURKs (AURK A, B, and C) with AURKB and AURKC showing structural and functional similarities. To delineate the meiotic roles of these three mammalian AURKs in mice, we have used a combination of chemical and genetic approaches to abrogate AURK activity at various stages of meiotic prophase I. By inducing wild type spermatocytes to undergo the G2/MI transition with okadaic acid (OA) in the presence of specific AURK inhibitors, we have determined a functional role for AURKB and AURKC in initiating desynapsis disassembly of the lateral element component of the SC, SYCP3. Cells treated with AURKB/C inhibitors failed to disassemble SYCP3 stretches and were unable to complete the G2/MI transition. This phenotype was not observed in cells treated with a specific AURKA inhibitor. To gain further insight in the functions of AURKB and AURKC during spermatogenesis, novel STOCK-Aurkbtm2.1Mama Tg(Spo11-cre)1Rsw or Tg(Hspa2-cre)1Eddy conditional knockout mice and B6;129S5-Aurkctm1Lex knockout mice were characterized. Despite defects being observed in histological sections of testes as well as aberrancies in spindle morphology of metaphase cells, both AURKB and AURKC mutant mice were fertile. This work supports the meiotic specific function of AURKB and AURKC in the disassembly of the SC during the G2/MI transition, and implies that these two kinases may play functionally compensatory roles in mammalian meiosis. Our current work is focusing on assessing STOCK- Aurkctm1Lex , Aurkbtm2.2Mama double knockout mice to further evaluate the meiotic specific functions of the aurora kinases, and improve our understanding of meiotically derived human disorders such as defects that can result in infertility, miscarriage, and developmental abnormalities.