Even a well-studied gene might have important functions in development that are masked by contributions of other genes. MEL-28/ELYS plays key roles in post-mitotic rebuilding of the nuclear envelope and in chromosome segregation. In C. elegans
mel-28 mutants show strict maternal-effect lethality, suggesting that MEL-28 is required in the embryo but is dispensable post-embryonically. To identify post-embryonic roles for MEL-28, we performed an RNAi-based genetic interaction screen, seeking genes that cause novel phenotypes in the
mel-28 mutant background. We identified multiple interactors, including genes that encode components of dynein, a minus-end directed motor responsible for the movements of multiple intracellular cargoes, and dynactin, a complex that helps couple dynein to its cargo. To characterize the interactions, we generated double mutants between
mel-28 and
dhc-1 (which encodes the heavy chain of dynein) or
dnc-1 (which encodes the
p150 subunit of dynactin).
dhc-1;
mel-28 double mutants produce a drastically reduced brood size compared to each single mutant. In addition,
dhc-1;
mel-28 males are infertile, and hermaphrodites have a disorganized proximal gonad and ovulation defects. None of these defects are present in either of the single mutants, suggesting that
mel-28 and
dhc-1 redundantly contribute to germ-line function. The
dnc-1 single mutant has a decreased brood size compared to the wild type and lays many unfertilized oocytes, suggesting defects with fertilization. Disruption of
mel-28 rescues the brood size and fertilization defects of
dnc-1 animals. This suggests that the dynactin complex and MEL-28 act antagonistically in C. elegans fertilization. In conclusion, we have shown that MEL-28 activities intersect with dynein and dynactin in the gonad, and in so doing we have revealed a novel role for MEL-28 in C. elegans fertility.