Fibronectin, mesoderm migration, and gastrulation in Xenopus
Fibronectin, mesoderm migration, and gastrulation in Xenopus
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DOI：
10.1006/dbio.1996.0174
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发表时间：
1996-08-01
影响因子：
2.7
通讯作者：
Keller, RE
中科院分区：
文献类型：
--
作者：
Winklbauer, R;Keller, RE
纤维连接蛋白在中胚层细胞迁移中的作用，以及中胚层迁移对非洲爪哇原肠形成的重要性进行了研究。为了允许迁移，迁移的中胚层细胞和基底层的细胞，即胚囊顶层之间必须存在稳定的界面。我们证明这种界面的维持不依赖于纤维连接蛋白。我们进一步证明，纤维连接蛋白有助于中胚层细胞与胚泡顶端的黏附，但不是必需的。然而，与纤维连接蛋白的相互作用是细胞扩散和形成片状细胞质突起所必需的。显然，纤维连接蛋白在中胚层迁移中的特殊作用是控制细胞的突起活动。因此，当纤维连接蛋白功能被GRGDSP多肽或抗体阻断时，中胚层细胞的迁移受到抑制。然而，在用抑制剂处理的胚胎中，原肠发育几乎正常进行。在非洲爪蛙中，中胚层的迁移似乎不是原肠发育所必需的。(C)1996年学术出版社。
The role of fibronectin in mesoderm cell migration and and the importance of mesoderm migration for gastrulation in Xenopus are examined. To allow for migration, a stable interface must exist between migrating mesoderm cells and the cells of the substrate layer, the blastocoel roof. We show that maintenance of this interface does not depend on fibronectin. We further demonstrate that fibronectin contributes to, but is not essential for, mesoderm cell adhesion to the blastocoel roof. However, interaction with fibronectin is necessary for cell spreading and the formation of lamelliform cytoplasmic protrusions. Apparently, the specific role of fibronectin in mesoderm migration is to control cell protrusive activity. Consequently, when fibronectin function is blocked by GRGDSP peptide or antibodies, mesoderm cell migration is inhibited. Nevertheless, gastrulation proceeds nearly normally in inhibitor-treated embryos. It appears that in Xenopus, mesoderm migration is not essential for gastrulation. (C) 1996 Academic Press, Inc.