원문정보
초록
영어
Zinc plays an essential role in mammalian oocyte maturation, fertilization, and early embryogenesis. The zinc concentration increases during oocyte maturation, but decreases soon after fertilization. Depletion of zinc impairs various stages of oocyte maturation, including cell cycle control, asymmetric division, and cytokinesis. However, the exact mechanisms by which zinc is involved in these processes is unknown. Here, we report that zinc, via the actin nucleator Spire, acts as an essential regulator of the actin cytoskeleton remodeling during mouse oocyte maturation and fertilization. Depletion of zinc in the mouse oocyte by either chemical chelation or knockdown of zinc transporters impaired cortical and cytoplasmic actin formation. Spire colocalized with zinccontaining vesicles via its FYVE domain, which contains zinc finger motifs that are essential for proper localization: mutation of zinc-binding cysteines in the FYVE domain abolished proper localization and actin mesh formation in oocytes. Expression of Spire truncation mutants revealed that all three major domains of the actin nucleator are required for correct localization and activity. After fertilization/parthenogenetic activation, Spire localization was dramatically altered following zinc release from the oocyte. Collectively, our data reveal novel roles for zinc in the regulation of the actin nucleator Spire and suggest a novel mechanism for the transition from asymmetric to symmetric cell division during mammalian oocyte maturation and fertilization.