Chromosome segregation errors during meiosis are the leading cause of aneuploidy. Faithful chromosome segregation during meiosis in most eukaryotes requires a crossover which provides a physical attachment holding homologs together in a "bivalent". Crossovers are critical for homologs to be properly aligned and partitioned in the first meiotic division. Without a crossover, individual homologs (univalents) might segregate randomly, resulting in aneuploid progeny. However, C. elegans
zim-2 mutants, which have crossover defects on chromosome V, have fewer dead embryos than expected from random segregation. This deviation from random segregation is more pronounced in
zim-2 males than in females. We found three phenomena that can explain this apparent discrepancy. First, we detected crossovers on chromosome V in both
zim-2(
tm574) oocytes and spermatocytes, suggesting a redundant mechanism to make up for the ZIM-2 loss. Second, after accounting for the background crossover frequency, spermatocytes produced significantly more euploid gametes than would be expected from random segregation. Lastly, trisomy of chromosome V is viable and fertile. Together, these three phenomena allow
zim-2(
tm574) mutants with reduced crossovers on chromosome V to have more viable progeny. Furthermore, live imaging of meiosis in
spo-11(
me44) oocytes and spermatocytes, which exhibit crossover failure on all six chromosomes, showed 12 univalents segregating apart in roughly equal masses in a homology independent manner, supporting the existence of a mechanism that segregates any two chromosomes apart.