Closure of the posterior neuropore in the vl mutant mouse.

Alterations in the surface topography of cells in the apical neural folds of the posterior neuropore were analyzed by means of scanning electron microscopy in normal (+/+) and abnormal (vl/vl) embryos characterized by lumbosacral dysraphism. In early embryos (14-25 somites) surface features distinguishing the neuroepithelial cells, transitional zone cells, and surface ectoderm cells were similar in normal and abnormal embryos, as were the arrangement and configuration of filopodia and lamellipodia. However, in embryos with approximately 26-36 somites, the transitional zone of the abnormals showed a profusion of large blebs and excrescences along the entire length of the posterior neuropore. By 36 somites, the posterior neuropore was still variably open in the abnormals, in contrast to normal embryos in which no external opening could be detected. In view of the abnormalities associated with the transitional zone, it is possible that the underlying mechanism that results in lumbosacral spina bifida in this mutant may involve putative neural crest cells.