Our results demonstrate that in mice, the primary meiotic function of TRIP13 is in recombination itself. We found no evidence that it is involved in pachytene checkpoint control. Our data suggest that while recombination events destined to be resolved as COs can proceed normally in Trip13 mutants, DSBs that enter the NCO repair pathway are incompletely resolved or processed inefficiently. This hypothesis is compatible with current knowledge of meiotic recombination pathways. In S. cerevisiae, CO and NCO pathways are distinct [43]; they have different recombination intermediates, and are dependent upon different proteins [44,45]. Mice also appear to have independent CO versus NCO recombination pathways [46]. As in yeast, both require SPO11-induced breaks, but only the CO pathway requires MLH1. Both types of recombinant products are formed by mid-late pachynema. Another possibility is that the recombination defects are a result of defective intersister recombination. However, this type of DSB repair is suppressed in meiotic cells. Ablation of RAD54, which mediates intersister recombination in yeast, does not significantly disrupt meiosis in either yeast or mice [47,48]. Interestingly, RAD54-deficient spermatocytes display abnormal persistence of RAD51 foci on pachytene chromosomes, similar to those in TRIP13 mice, but there are no deleterious effects on meiotic progression or fertility [49].