The cortex controls cell shape. In mouse oocytes, the cortex thickens in an Arp2/3-complex-dependent manner, ensuring chromosome positioning and segregation. Surprisingly, we identify that mouse oocytes lacking the Arp2/3 complex undergo cortical actin remodeling upon division, followed by cortical contractions that are unprecedented in mammalian oocytes. Using genetics, imaging, and machine learning, we show that these contractions stir the cytoplasm, resulting in impaired organelle organization and activity. Oocyte capacity to avoid polyspermy is impacted, leading to a reduced female fertility. We could diminish contractions and rescue cytoplasmic anomalies. Similar contractions were observed in human oocytes collected as byproducts during IVF (in vitro fertilization) procedures. These contractions correlate with increased cytoplasmic motion, but not with defects in spindle assembly or aneuploidy in mice or humans. Our study highlights a multiscale effect connecting cortical F-actin, contractions, and cytoplasmic organization and affecting oocyte quality, with implications for female fertility.

皮质控制细胞形状。在小鼠卵母细胞中，皮质以 Arp2/3 复合物依赖性方式增厚，确保染色体定位和分离。令人惊讶的是，我们发现缺乏 Arp2/3 复合物的小鼠卵母细胞在分裂时经历皮质肌动蛋白重塑，随后发生哺乳动物卵母细胞中前所未有的皮质收缩。利用遗传学、成像和机器学习，我们发现这些收缩会搅动细胞质，导致细胞器组织和活动受损。卵母细胞避免多精的能力受到影响，导致女性生育能力下降。我们可以减少收缩并挽救细胞质异常。在 IVF（体外受精）过程中作为副产品收集的人类卵母细胞中也观察到类似的收缩。这些收缩与细胞质运动的增加相关，但与小鼠或人类的纺锤体组装或非整倍性缺陷无关。我们的研究强调了皮质 F-肌动蛋白、收缩和细胞质组织之间的多尺度效应，并影响卵母细胞质量，从而影响女性生育能力。