Tanaka Yosuke, Okada Yasushi, Hirokawa Nobutaka
Department of Cell Biology and Anatomy, Graduate School of Medicine, University of Tokyo, Hongo, Tokyo 113-0033, Japan.
Nature. 2005 May 12;435(7039):172-7. doi: 10.1038/nature03494.
The precise specification of left-right asymmetry is an essential process for patterning internal organs in vertebrates. In mouse embryonic development, the symmetry-breaking process in left-right determination is initiated by a leftward extraembryonic fluid flow on the surface of the ventral node. However, it is not known whether the signal transduction mechanism of this flow is chemical or mechanical. Here we show that fibroblast growth factor (FGF) signalling triggers secretion of membrane-sheathed objects 0.3-5 microm in diameter termed 'nodal vesicular parcels' (NVPs) that carry Sonic hedgehog and retinoic acid. These NVPs are transported leftward by the fluid flow and eventually fragment close to the left wall of the ventral node. The silencing effects of the FGF-receptor inhibitor SU5402 on NVP secretion and on a downstream rise in Ca2+ were sufficiently reversed by exogenous Sonic hedgehog peptide or retinoic acid, suggesting that FGF-triggered surface accumulation of cargo morphogens may be essential for launching NVPs. Thus, we propose that NVP flow is a new mode of extracellular transport that forms a left-right gradient of morphogens.
左右不对称的精确设定是脊椎动物内脏器官模式形成的关键过程。在小鼠胚胎发育过程中,左右决定的对称性打破过程由腹侧节点表面向左的胚外液流启动。然而,尚不清楚这种液流的信号转导机制是化学性的还是机械性的。在此,我们表明成纤维细胞生长因子(FGF)信号传导触发直径为0.3 - 5微米的膜包裹物体(称为“节点囊泡包裹体”,NVPs)的分泌,这些包裹体携带音猬因子和视黄酸。这些NVPs被液流向左运输,最终在腹侧节点左壁附近破碎。FGF受体抑制剂SU5402对NVP分泌和下游Ca2 +升高的沉默作用可被外源性音猬因子肽或视黄酸充分逆转,这表明FGF触发的货物形态发生素的表面积累可能是启动NVPs所必需的。因此,我们提出NVP流是一种新的细胞外运输模式,它形成形态发生素的左右梯度。