A cellular framework for gut-looping morphogenesis in zebrafish
A cellular framework for gut-looping morphogenesis in zebrafish
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DOI：
10.1126/science.1085397
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发表时间：
2003-10-24
期刊：
影响因子：
56.9
通讯作者：
Stainier, DYR
中科院分区：
文献类型：
--
作者：
Horne-Badovinac, S;Rebagliati, M;Stainier, DYR
许多脊椎动物的器官采用不对称的位置相对于中线，但很少有人知道的细胞变化和组织运动，发生下游的左右基因表达，以产生这种不对称。在这里，我们提供的证据表明，循环的斑马鱼肠道结果从相邻的侧板中胚层（LPM）的不对称迁移。破坏LPM上皮结构的突变会扰乱这种不对称迁移并抑制肠循环。不对称的LPM迁移仍然发生时，内胚层从肠循环区域消融，这表明LPM可以自主地提供动力的肠道位移。最后，减少左侧Nodal活动会随机化LPM迁移和肠道循环的模式。这些结果揭示了不对称表达基因调控器官偏侧性的细胞框架。
Many vertebrate organs adopt asymmetric positions with respect to the midline, but little is known about the cellular changes and tissue movements that occur downstream of left-right gene expression to produce this asymmetry. Here, we provide evidence that the looping of the zebrafish gut results from the asymmetric migration of the neighboring lateral plate mesoderm (LPM). Mutations that disrupt the epithelial structure of the LPM perturb this asymmetric migration and inhibit gut looping. Asymmetric LPM migration still occurs when the endoderm is ablated from the gut-looping region, suggesting that the LPM can autonomously provide a motive force for gut displacement. Finally, reducing left-sided Nodal activity randomizes the pattern of LPM migration and gut looping. These results reveal a cellular framework for the regulation of organ laterality by asymmetrically expressed genes.