Proper left–right symmetry breaking is essential for animal development, and in many cases, this process is actomyosin-dependent. In Caenorhabditis elegans embryos active torque generation in the actomyosin layer promotes left–right symmetry breaking by driving chiral counterrotating cortical flows. While both Formins and Myosins have been implicated in left–right symmetry breaking and both can rotate actin filaments in vitro, it remains unclear whether active torques in the actomyosin cortex are generated by Formins, Myosins, or both. We combined the strength of C. elegans genetics with quantitative imaging and thin film, chiral active fluid theory to show that, while Non-Muscle Myosin II activity drives cortical actomyosin flows, it is permissive for chiral counterrotation and dispensable for chiral symmetry breaking of cortical flows. Instead, we find that CYK-1/Formin activation in RhoA foci is instructive for chiral counterrotation and promotes in-plane, active torque generation in the actomyosin cortex. Notably, we observe that artificially generated large active RhoA patches undergo rotations with consistent handedness in a CYK-1/Formin–dependent manner. Altogether, we conclude that CYK-1/Formin–dependent active torque generation facilitates chiral symmetry breaking of actomyosin flows and drives organismal left–right symmetry breaking in the nematode worm.

适当的左右对称破坏对动物发育至关重要，在许多情况下，这个过程依赖于肌动球蛋白。在秀丽隐杆线虫胚胎中，肌动球蛋白层中的主动扭矩产生通过驱动手性反向旋转皮层流动来促进左右对称性破坏。虽然 Formins 和 Myosins 都与左右对称性破坏有关，并且两者都可以在体外旋转肌动蛋白丝，但目前尚不清楚肌动球蛋白皮层中的主动扭矩是由 Formins、肌球蛋白还是两者产生的。我们结合了秀丽隐杆线虫的力量遗传学与定量成像和薄膜、手性活性流体理论表明，虽然非肌肉肌球蛋白 II 活性驱动皮质肌动球蛋白流动，但它允许手性反向旋转，并且对于皮质流动的手性对称性破坏是可有可无的。相反，我们发现 RhoA 病灶中的 CYK-1/Formin 激活对手性反向旋转具有指导意义，并促进肌动球蛋白皮层中的平面内主动扭矩生成。值得注意的是，我们观察到人工生成的大型活性 RhoA 斑块以依赖于 CYK-1/Formin 的方式以一致的手性进行旋转。总而言之，我们得出结论，CYK-1/Formin 依赖的主动扭矩产生促进了肌动球蛋白流的手性对称性破坏，并驱动了线虫蠕虫中生物体左右对称性的破坏。