Our research focuses on the evolutionarily conserved process of meiosis, using C. elegans as a model system. Meiosis enables sexual reproduction by the production of haploid gametes. A successful meiotic division relies on the formation of crossover events between each pair of homologous chromosomes. These crossover events are formed in the context of the synaptonemal complex (SC), a protein complex that bridges paired homologous chromosomes during meiotic prophase I.  Hence, in the absence of a functional SC, meiosis is abrogated. Perturbation of meiosis can lead to chromosome nondisjunction, which is the leading cause for miscarriages and birth defects in humans. These observations, combined with evidence from studies of infertile patients, suggest a connection between SC dysfunction and chromosomal nondisjunction in human reproduction. In our lab we aim to discover and characterize novel genes essential for various aspects of meiosis, including genes essential for chromosome pairing, recombination, and the regulation of SC assembly and disassembly. To accomplish this goal, we are engaged in genetic screens targeted to isolate genes in these processes. This approach has already resulted in the identification of a novel class of mutants affecting SC disassembly. We combine our genetic approaches with high-resolution microscopy to investigate the role of these proteins in meiosis. These studies will result in a better understanding of the various fundamental processes unfolding in C. elegans meiosis and will lead to insights into this basic process in other organisms as well. In-depth investigation of meiosis is of central importance for progress in developing methods to prevent and treat infertility and birth defects stemming from meiotic chromosome nondisjunction in humans.