Grima Ramon, Schnell Santiago
Complex Systems Group, Indiana University School of Informatics and Biocomplexity Institute, Eigenmann Hall 906, 1900 East Tenth Street, Bloomington, IN 47406, USA.
Dev Biol. 2007 Jul 15;307(2):248-57. doi: 10.1016/j.ydbio.2007.04.032. Epub 2007 May 3.
The prevailing model of somitogenesis supposes that the presomitic mesoderm is segmented into somites by a clock and wavefront mechanism. During segmentation, mesenchymal cells undergo compaction, followed by a detachment of the presumptive somite from the rest of the presomitic mesoderm and the subsequent morphological changes leading to rounded somites. We investigate the possibility that minimization of tissue surface tension drives the somite sculpting processes. Given the time in which somite formation occurs and the high bulk viscosities of tissues, we find that only small changes in shape and form of tissue typically occur through cell movement driven by tissue surface tension. This is particularly true for somitogenesis in the zebrafish. Hence it is unlikely that such processes are the sole and major driving force behind somite formation. We propose a simple chemotactic mechanism that together with heightened adhesion can account for the morphological changes in the time allotted for somite formation.
当前的体节发生模型认为，前体中胚层是通过时钟和波前机制分割成体节的。在分割过程中，间充质细胞会发生压实，随后假定的体节与前体中胚层的其余部分分离，接着发生形态变化，形成圆形的体节。我们研究了组织表面张力最小化驱动体节塑造过程的可能性。考虑到体节形成发生的时间以及组织的高体积粘度，我们发现，通常只有通过组织表面张力驱动的细胞运动，组织的形状和形态才会发生微小变化。斑马鱼的体节发生尤其如此。因此，这些过程不太可能是体节形成背后唯一的主要驱动力。我们提出了一种简单的趋化机制，该机制与增强的黏附作用一起，可以解释在分配给体节形成的时间内发生的形态变化。
