Aneuploidy is the leading cause of birth defects and spontaneous abortions in humans. The majority of aneuploidies are maternally derived, and most of the clinically relevant cases arise from segregation errors in meiosis I. During meiosis I, key steps leading to the formation of a stable bivalent must be undertaken with precision in order to ensure proper segregation of homologous chromosomes. In our research we use the zebrafish, Danio rerio, to comparatively study early meiotic processes in males and females with the goal of understanding which factors contribute to aneuploidy generation in the two sexes. A thorough examination of these processes has been hindered in mammals by the limited accessibility of female oocytes going through early prophase I. In zebrafish, however, the gonad is transparent and easily accessible, and germ cells in both males and females undergo meiosis throughout their lives (Draper, McCallum and Moens, 2007). While previous studies have shown telomere clustering and Sycp3 loading in zebrafish males (Saito K et al., 2011 and 2014), there are still many unanswered questions. Most notably there has not been a thorough study of how zebrafish male and female meioses differ, and how the two sexes respond to perturbations in meiosis. We have created loss of function mutations in genes with key roles in meiotic chromosome dynamics. The first is in spo11, which encodes the nuclease that generates programmed double strand breaks which initiate homologous recombination. The second is in rad21l1 that encodes a meiosis-specific cohesin subunit found only in vertebrates. Both spo11 and rad21l1 mutants have sexually dimorphic phenotypes. While spo11 males are completely infertile and lack sperm, the spo11 females are fertile but most of their offspring are highly deformed and aneuploid. The rad21l1 mutants by contrast have a defect in maintaining the female phenotype with over 97% of homozygotes developing into males which appear to be fully fertile. Interestingly, in rad21l1/tp53 double mutants, the defect in maintaining femaleness is rescued but most of the double mutant females’ offspring are deformed. This phenotype is distinctly different from the spo11 aneuploid offspring, suggesting the defects may be due to some other lesion not related to aneuploidy. Together, our results support zebrafish as a coherent model that demonstrates both similarities and differences between meiosis in the two sexes.