Rapid epithelial tissue flows are essential to building and shaping developing embryos. However, the mechanical properties of embryonic epithelial tissues and the factors that control these properties are not well understood. Actomyosin generates contractile tensions and contributes to the mechanical properties of cells and cytoskeletal networks in vitro, but it remains unclear how the levels and patterns of actomyosin activity contribute to embryonic epithelial tissue mechanics in vivo. To dissect the roles of cell-generated tensions in the mechanics of flowing epithelial tissues, we use optogenetic tools to manipulate actomyosin contractility with spatiotemporal precision in the Drosophila germband epithelium, which rapidly flows during body axis elongation. We find that manipulating actomyosin-dependent tensions by either optogenetic activation or deactivation of actomyosin alters the solid-fluid mechanical properties of the germband epithelium, leading to changes in cell rearrangements and tissue-level flows. Optogenetically activating actomyosin leads to increases in the overall level but decreases in the anisotropy of tension in the tissue, whereas optogenetically deactivating actomyosin leads to decreases in both the level and anisotropy of tension compared to in wild-type embryos. We find that optogenetically activating actomyosin results in more solidlike (less fluidlike) tissue properties, which is associated with reduced cell rearrangements and tissue flow compared to in wild-type embryos. Optogenetically deactivating actomyosin also results in more solidlike properties than in wild-type embryos but less solidlike properties compared to optogenetically activating actomyosin. Together, these findings indicate that increasing the overall tension level is associated with more solidlike properties in tissues that are relatively isotropic, whereas high-tension anisotropy fluidizes the tissue. Our results reveal that epithelial tissue flows in developing embryos involve the coordinated actomyosin-dependent regulation of the mechanical properties of tissues and the tensions driving them to flow in order to achieve rapid tissue remodeling.

Sperm swimming is crucial to fertilize the egg, in nature and in assisted reproductive technologies. Modeling the sperm dynamics involves elasticity, hydrodynamics, internal active forces, and out-of-equilibrium noise. Here we give experimental evidence in favor of the relevance of energy dissipation for sperm beating fluctuations. For each motile cell, we reconstruct the time evolution of the two main tail's spatial modes, which together trace a noisy limit cycle characterized by a maximum level of precision $p_{\text{max}}$. Our results indicate $p_{\text{max}}\sim {10}^2{\text{s}}^{-1}$, remarkably close to the estimated precision of a dynein molecular motor actuating the flagellum, which is bounded by its energy dissipation rate according to the thermodynamic uncertainty relation. Further experiments under oxygen deprivation show that $p_{\text{max}}$ decays with energy consumption, as it occurs for a single molecular motor. Both observations are explained by conjecturing a high level of coordination among the conformational changes of dynein motors. This conjecture is supported by a theoretical model for the beating of an ideal flagellum actuated by a collection of motors, including a motor-motor nearest-neighbor coupling of strength $K$: When $K$ is small the precision of a large flagellum is much higher than the single motor one. On the contrary, when $K$ is large the two become comparable. Based upon our strong-motor-coupling conjecture, old and new data coming from different kinds of flagella can be collapsed together on a simple master curve.