To study the roles of dynactin and the MEL-28 protein in C. elegans fertility, we analyzed animals homozygous for loss-of-function mutations in genes affecting each of two proteins. Specifically, we studied
dnc-1(or 404) a temperature-sensitive mutation impacting the
p150 glued subunit of dynactin, and
mel-28(
t1684) a null mutation that destroys the MEL-28 protein product. Dynactin is a protein complex that connects microtubule motors dynein and kinesin to their cargo and is thus essential for intracellular transport. The
mel-28 gene encodes a protein that rebuilds the nuclear pore after cell division and is also important for chromosome segregation.
dnc-1 mutants have a significantly decreased brood size and produce many unfertilized oocytes, which suggests a problem with the sperm. To test the hypothesis that the
dnc-1 mutants have defective sperm, we set up sperm competition tests that found significant differences in sperm functionality between
dnc-1 mutant males and normal males. When an animal has both the
dnc-1 and
mel-28 mutations, the sperm defects are recovered. Our current goal is to further study how the sperm is impacted by the
dnc-1 mutation and why defects to the
mel-28 gene rescue these defects. Dynactin and MEL-28 are important in all animal cells, so studying nematode fertility will eventually lead to a better understanding of how human cells work too.