Global tissue tension anisotropy has been shown to trigger stereotypical cell division orientation by elongating mitotic cells along the main tension axis. Yet, how tissue tension elongates mitotic cells despite those cells undergoing mitotic rounding (MR) by globally upregulating cortical actomyosin tension remains unclear. We addressed this question by taking advantage of ascidian embryos, consisting of a small number of interphasic and mitotic blastomeres and displaying an invariant division pattern. We found that blastomeres undergo MR by locally relaxing cortical tension at their apex, thereby allowing extrinsic pulling forces from neighboring interphasic blastomeres to polarize their shape and thus division orientation. Consistently, interfering with extrinsic forces by reducing the contractility of interphasic blastomeres or disrupting the establishment of asynchronous mitotic domains leads to aberrant mitotic cell division orientations. Thus, apical relaxation during MR constitutes a key mechanism by which tissue tension anisotropy controls stereotypical cell division orientation.

已显示全局组织张力各向异性通过沿主张力轴拉长有丝分裂细胞来触发定型细胞分裂方向。然而，尽管这些细胞通过全局上调皮质肌动球蛋白张力进行有丝分裂圆化 (MR)，但组织张力如何延长有丝分裂细胞仍不清楚。我们通过利用海鞘胚胎来解决这个问题，海鞘胚胎由少量间期和有丝分裂卵裂球组成，并显示出不变的分裂模式。我们发现卵裂球通过在其顶端局部松弛皮质张力来进行 MR，从而允许来自相邻间期卵裂球的外在拉力使其形状极化，从而使分裂方向极化。始终如一，通过降低间期卵裂球的收缩性或破坏异步有丝分裂域的建立来干扰外力会导致异常的有丝分裂细胞分裂方向。因此，MR 期间的顶端松弛构成了组织张力各向异性控制定型细胞分裂方向的关键机制。