It is clear that there are many genes required for meiosis in mammals that are not present in the more tractable model organisms. To identify such genes, our lab has performed forward genetic chemical (ENU) mutagenesis screens for alleles conferring infertility in mice. A novel allele, Ccnb1ip1mei4, generated in these screens is of interest because it is defective in a form of recombination called crossing-over. Ccnb1ip1mei4/mei4 results in male and female infertility of otherwise normal-appearing animals. CCNB1IP1 is finely regulated in both timing and localization to the events of meiotic crossover formations. Towards understanding the molecular functions of CCNB1IP1 and how the defect in Ccnb1ip1me4i/mei4 animals leads to meiotic arrest, studies of CCNB1IP1 within meiocytes implicate a role for CCNB1IP1 in SUMOylation. Remarkably little is understood about SUMO-modification consequences to meiosis. Protein-protein interactions with CCNB1IP1 identify a number of putative targets of SUMOylation, and subsequent in vivo biochemical interrogations reveal the CCNB1IP1-interacting proteins 4930455F23RIK and GGN as targets of posttranslational modification dependent upon a putative SUMO E3 ligase. In totality, these studies support the hypothesis that CCNB1IP1 performs as a meiotic coregulator, mediating the SUMO-modification of proteins essential to the stabilization and maturation of crossover intermediates. These studies of CCNB1IP1 point towards a better understanding of meiosis, with emphasis upon new targets and roles of SUMOylation.