Chromosomal abnormalities in oocytes are a leading cause of miscarriage and genetic disorders of the fetus. A major underlying cause of these abnormalities is defects in meiotic crossover (CO) formation. To achieve COs, the topoisomerase-like enzyme, SPO-11, creates DNA double strand breaks (DSBs), allowing for repair of those breaks by homologous recombination. COs can be seen as chiasmata that help to correctly orient chromosomes on the spindle during metaphase I for proper segregation. Therefore, without DSBs and subsequent CO events, chromosomes risk missegregation. By understanding the components of DSB formation, we gain insight into events in recombination and the creation of COs with their associated chiasmata. Nevertheless, our understanding of the protein complexes that regulate DSB formation is lacking. Caenorhabditis elegans is ideal for the study of meiosis, DSBs, and aneuploidy given its ease of genetic manipulation and shared meiotic characteristics with women. By analyzing double mutants of genes involved in DSBs, we can build networks of the genetic interactions required for DSB formation. We have analyzed a matrix of interactions between partial loss-of-function alleles of genes involved in DSB formation in C. elegans. These include mutations in lin-35, cep-1, dsb-2, rec-1, him-17, him-5, parg-1, and mre-11. We then analyzed diakinesis oocytes by whole mount staining followed by confocal microscopy and 3D visualization. Assessment of achiasmate chromosomes has allowed us to determine synthetic interactions for CO formation in these sets of mutants. We also analyzed the effects of the mutations on brood size and frequency of males. Preliminary analysis suggests that the DSB genes fall into multiple groups that interact synergistically to impact break formation. .