Human and mouse oocytes’ developmental potential can be predicted by their mechanical properties. Their development into blastocysts requires a specific stiffness window. In this study, we combine live-cell and computational imaging, laser ablation, and biophysical measurements to investigate how deregulation of cortex tension in the oocyte contributes to early developmental failure. We focus on extra-soft cells, the most common defect in a natural population. Using two independent tools to artificially decrease cortical tension, we show that chromosome alignment is impaired in extra-soft mouse oocytes, despite normal spindle morphogenesis and dynamics, inducing aneuploidy. The main cause is a cytoplasmic increase in myosin-II activity that could sterically hinder chromosome capture. We describe here an original mode of generation of aneuploidies that could be very common in oocytes and could contribute to the high aneuploidy rate observed during female meiosis, a leading cause of infertility and congenital disorders.

人和小鼠卵母细胞的发育潜力可以通过其机械性能来预测。它们发展为胚泡需要特定的硬度窗口。在这项研究中，我们结合了活细胞和计算成像，激光消融和生物物理测量，以研究卵母细胞中皮质张力的失调如何导致早期发育衰竭。我们专注于超软细胞，这是自然种群中最常见的缺陷。使用两个独立的工具人为地降低皮质张力，我们显示，尽管正常的纺锤体形态发生和动力学，诱导非整倍性，超软小鼠卵母细胞的染色体排列受到损害。主要原因是肌球蛋白II活性的细胞质增加，可能在空间上阻碍染色体捕获。