Gammill Laura S, Gonzalez Constanza, Bronner-Fraser Marianne
Division of Biology 139-74, California Institute of Technology, Pasadena, California 91125, USA.
Dev Neurobiol. 2007 Jan;67(1):47-56. doi: 10.1002/dneu.20326.
In the head of vertebrate embryos, neural crest cells migrate from the neural tube into the presumptive facial region and condense to form cranial ganglia and skeletal elements in the branchial arches. We show that newly formed neural folds and migrating neural crest cells express the neuropilin 2 (npn2) receptor in a manner that is highly conserved in amniotes. The repulsive npn2 ligand semaphorin (sema) 3F is expressed in a complementary pattern in the mouse. Furthermore, mice carrying null mutations for either npn2 or sema3F have abnormal cranial neural crest migration. Most notably, "bridges" of migrating cells are observed crossing between neural crest streams entering branchial arches 1 and 2. In addition, trigeminal ganglia fail to form correctly in the mutants and are improperly condensed and loosely organized. These data show that npn2/sema3F signaling is required for proper cranial neural crest development in the head.
在脊椎动物胚胎的头部，神经嵴细胞从神经管迁移至假定的面部区域，并聚集形成鳃弓中的颅神经节和骨骼成分。我们发现，新形成的神经褶和迁移的神经嵴细胞以一种在羊膜动物中高度保守的方式表达神经纤毛蛋白2（npn2）受体。排斥性npn2配体信号素（sema）3F在小鼠中以互补模式表达。此外，npn2或sema3F基因敲除的小鼠颅神经嵴迁移异常。最显著的是，观察到迁移细胞的“桥”在进入鳃弓1和鳃弓2的神经嵴流之间交叉。此外，突变体中的三叉神经节未能正常形成，且聚集不当、组织松散。这些数据表明，npn2/sema3F信号传导是头部正常颅神经嵴发育所必需的。
