In many animals, sperm cells are held in an inactive form for energy conservation and are rapidly activated when motility is required. Now, Chieh-Hsiang Tan and Kerry Kornfeld show that increases in cytosolic zinc levels are sufficient to activate sperm in C. elegans. Previous work in C. elegans has identified two signalling pathways implicated in sperm activation. The first pathway is dependent on TRY-5, a secreted protease, and its candidate target, the cell surface protein SNF-10, whereas the second pathway involves the SPE-8 group of proteins and ZIPT-7.1, a ZIP family cation transporter. In this study, the authors confirm that the addition of extracellular zinc is sufficient to activate both wild-type and snf-10 mutant sperm, but not the sperm of zipt-7.1 or spe-8 mutants. However, addition of the zinc ionophore pyrithione (which binds zinc and transports it across cellular membranes) alongside extracellular zinc activates sperm in vitro and bypasses the activation defect observed in zipt-7.1(lf) and spe-8(lf) mutants, implicating SPE-8, as well as ZIPT-7.1, in zinc transport across membranes. These results, together with previous data demonstrating a role for zinc in human fertility, could have implications for in vitro activation of human sperm and new approaches for treating infertility.
