Actomyosin‐mediated apical constriction drives a wide range of morphogenetic processes. Activation of myosin‐II initiates pulsatile cycles of apical constrictions followed by either relaxation or stabilization (ratcheting) of the apical surface. While relaxation leads to dissipation of contractile forces, ratcheting is critical for the generation of tissue‐level tension and changes in tissue shape. How ratcheting is controlled at the molecular level is unknown. Here, we show that the actin crosslinker βH‐spectrin is upregulated at the apical surface of invaginating mesodermal cells during Drosophila gastrulation. βH‐spectrin forms a network of filaments which co‐localize with medio‐apical actomyosin fibers, in a process that depends on the mesoderm‐transcription factor Twist and activation of Rho signaling. βH‐spectrin knockdown results in non‐ratcheted apical constrictions and inhibition of mesoderm invagination, recapitulating twist mutant embryos. βH‐spectrin is thus a key regulator of apical ratcheting during tissue invagination, suggesting that actin cross‐linking plays a critical role in this process.

中文翻译：

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在组织内陷过程中，需要使用βH-血影蛋白来棘顶心尖搏动性收缩。

肌动球蛋白介导的根尖收缩驱动多种形态发生过程。肌球蛋白II的激活会引发心尖收缩的搏动周期，然后使心尖表面松弛或稳定（棘齿）。放松会导致收缩力的消散，而棘轮对于组织水平张力的产生和组织形状的改变至关重要。在分子水平上如何控制棘轮是未知的。在这里，我们表明果蝇期间肌动蛋白交联剂βH-血影蛋白在侵袭性中胚层细胞的顶表面上调。胃气化。βH-血影蛋白形成细丝网络，该细丝网络与中顶肌动球蛋白纤维共定位，其过程取决于中胚层转录因子Twist和Rho信号的激活。βH-spectrin的敲除可导致未棘突的根尖收缩并抑制中胚层的内陷，从而概括扭曲突变体的胚胎。因此，βH-血影蛋白是组织内陷过程中根尖棘齿的关键调节剂，表明肌动蛋白交联在此过程中起关键作用。