A key event at the onset of development is the activation of a contractile actomyosin cortex during the oocyte-to-embryo transition^1,2,3. Here we report on the discovery that, in Caenorhabditis elegans oocytes, actomyosin cortex activation is supported by the emergence of thousands of short-lived protein condensates rich in F-actin, N-WASP and the ARP2/3 complex^4,5,6,7,8 that form an active micro-emulsion. A phase portrait analysis of the dynamics of individual cortical condensates reveals that condensates initially grow and then transition to disassembly before dissolving completely. We find that, in contrast to condensate growth through diffusion⁹, the growth dynamics of cortical condensates are chemically driven. Notably, the associated chemical reactions obey mass action kinetics that govern both composition and size. We suggest that the resultant condensate dynamic instability¹⁰ suppresses coarsening of the active micro-emulsion¹¹, ensures reaction kinetics that are independent of condensate size and prevents runaway F-actin nucleation during the formation of the first cortical actin meshwork.

发育开始时的一个关键事件是在卵母细胞到胚胎的过渡过程中收缩肌动球蛋白皮质的激活^1,2,3。在这里，我们报告了以下发现：在秀丽隐杆线虫卵母细胞中，肌动球蛋白皮层的激活得到了数千种富含 F-肌动蛋白、N-WASP 和 ARP2/3 复合物的短寿命蛋白凝聚物的支持 4,5,6 ^{， 7,8}即形成活性微乳液。对单个皮质凝结物动力学的相图分析表明，凝结物最初生长，然后在完全溶解之前过渡到分解。^{我们发现，与通过扩散9 的}凝结水增长相反，皮质凝结物的生长动力学是化学驱动的。值得注意的是，相关的化学反应遵循控制成分和大小的质量作用动力学。我们认为由此产生的凝结物动态不稳定性¹⁰抑制了活性微乳液¹¹的粗化，确保了与凝结物大小无关的反应动力学，并防止在第一个皮质肌动蛋白网状结构形成过程中失控的 F-肌动蛋白成核。