AI 中文总结
该研究结合数学建模与活体成像发现，果蝇成神经细胞内陷依赖细胞内在机制而非组织流动性，揭示了发育系统维持关键过程稳健性的一种方式。
AI 中文摘要
形态发生涉及发育组织内多个细胞过程的协同作用。在果蝇胚胎发育早期，成神经细胞（NB）内陷与胚带延伸（GBE）同时发生，但这些过程是否存在机械相互作用尚不清楚。本研究结合数学建模与定量活体成像，探究GBE过程中的组织水平力学是否影响NB内陷动力学。数学建模预测，细胞重排受损导致组织流动性降低，会通过增加机械阻力减慢NB内陷速度。对细胞插入和GBE被破坏的突变体的实验分析显示，组织流动性显著降低。然而，当组织流动性下降时，NB内陷速率基本未受影响。将细胞内在的肌球蛋白各向异性和内吞作用-收缩耦合纳入数学模型，可恢复类固体组织中神经母细胞的内陷速率。因此，研究结果表明，维持内陷动力学的是细胞内在机制，而非组织水平的流动性。更广泛地说，这些结果说明发育系统可通过将关键细胞事件与组织水平力学变异性隔离开来，实现稳健性。
英文摘要
Morphogenesis involves the coordination of multiple cellular processes that occur simultaneously within developing tissues. During early Drosophila embryogenesis, neuroblast (NB) ingression occurs concurrently with germ band extension (GBE), yet whether these processes interact mechanistically remains unclear. Here, we combine mathematical modelling with quantitative live imaging to investigate whether tissue-level mechanics during GBE influence NB ingression dynamics. Mathematical modelling predicted that reducing tissue fluidity through impaired cellular rearrangements should slow NB ingression by increasing mechanical resistance. Experimental analysis of mutants in which cell intercalation and GBE are disrupted revealed a dramatic reduction in tissue fluidity. However, NB ingression rates remained largely unaffected when tissue fluidity decreased. Incorporating cell-intrinsic myosin anisotropy and endocytosis-contractility coupling into our mathematical model rescued the rate of neuroblast ingression in solid-like tissues. Thus, our findings suggest that cell-intrinsic mechanisms, rather than tissue-level fluidity, maintain ingression kinetics. More broadly, these results illustrate how developmental systems can achieve robustness by insulating critical cellular events from tissue-level mechanical variability.
