Forces Driving Epithelial Spreading in Zebrafish Gastrulation
Forces Driving Epithelial Spreading in Zebrafish Gastrulation
复制标题
DOI：
10.1126/science.1224143
复制
发表时间：
2012-10-12
期刊：
影响因子：
56.9
通讯作者：
Heisenberg, Carl-Philipp
中科院分区：
文献类型：
--
作者：
Behrndt, Martin;Salbreux, Guillaume;Heisenberg, Carl-Philipp
收缩肌球蛋白环驱动从胞质分裂到伤口愈合的各种基本形态发生过程。肌动球蛋白环通常被认为是通过周向收缩发挥作用的。在这里，我们展示了在斑马鱼原肠形成过程中，卵黄细胞上的包膜细胞层(EVL)的铺展是由收缩的肌球蛋白环驱动的。与以前的建议不同，我们发现这个环不仅通过周向收缩发挥作用，而且还通过流动摩擦机制发挥作用。这通过抵抗肌动球蛋白逆行流动产生拉力。在周向收缩无效的情况下，EVL扩散正常进行，这表明流动摩擦机制是足够的。因此，肌动球蛋白环可以通过缆索收缩和流动摩擦机制相结合的方式在上皮形态发生中发挥作用。
Contractile actomyosin rings drive various fundamental morphogenetic processes ranging from cytokinesis to wound healing. Actomyosin rings are generally thought to function by circumferential contraction. Here, we show that the spreading of the enveloping cell layer (EVL) over the yolk cell during zebrafish gastrulation is driven by a contractile actomyosin ring. In contrast to previous suggestions, we find that this ring functions not only by circumferential contraction but also by a flow-friction mechanism. This generates a pulling force through resistance against retrograde actomyosin flow. EVL spreading proceeds normally in situations where circumferential contraction is unproductive, indicating that the flow-friction mechanism is sufficient. Thus, actomyosin rings can function in epithelial morphogenesis through a combination of cable-constriction and flow-friction mechanisms.