Role for capping protein in mouse oocytes

Actin assembly is regulated by capping protein, which binds the barbed ends of actin filaments and terminates their elongation. This process is involved in the asymmetric division of mouse oocytes, but the role of capping protein itself is poorly understood. In this study (p. 160), Suk Namgoong, Nam-Hyung Kim and colleagues investigate the roles of capping protein at different stages of mouse oocyte maturation. The authors first show that capping protein mainly localises to the oocyte cytoplasm during maturation. Knockdown of capping protein impaired the asymmetric division of oocytes and increased the polar body size, suggesting that this protein is involved in spindle migration during oocyte migration. In addition, the authors observed a reduction in the cytoplasmic actin mesh in the absence of capping protein. Ectopic overexpression of capping protein also impaired asymmetric division and caused severe abnormalities in polar body extrusion. Time-lapse microscopy confirmed that knockdown or overexpression of capping protein impairs spindle migration and the timing of cytokinesis. Expression of the capping-protein-binding region of CARMIL, the capping-protein antagonist, decreased the oocyte maturation rate and cytoplasmic actin mesh density, further confirming the essential role of capping protein in oocyte maturation. Taken together, these data suggest that capping protein has an essential role in actin-driven processes during oocyte maturation.